CPG for Eating Disorders

Clinical Practice Guidelinefor Eating DisordersCLINICAL PRACTICE GUIDELINES IN THE NHS.MINISTRY OF HEALTHCARE AND CONSUMER AFFAIRS

CLINICAL PRACTICEGUIDELINE FOREATING DISORDERSCLINICAL PRACTICE GUIDELINES IN THE NHSMINISTRY OF HEALTHCARE AND CONSUMER AFFAIRS

This clinical practice guideline (CPG) is an aid for decision-making in health care. It is not in any way an obligedrequirement to adhere to every aspect of this CPG and it does not replace the clinical judgement of health careprofessionals.Edition: 1/February/2009Edited by: Catalan Agency for Health Technology Assessment and ResearchRoc Boronat, 81-9508005 BarcelonaNIPO: 477-08-022-8ISBN: 978-84-393-8010-8Legal Deposit: B-55481-2008© Ministry of Health and Consumer Affairs© Catalan Agency for Health Technology Assessment and Research3CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Table of ContentsPresentation 9Authors and Collaborations 11Key Questions 13CPG Recommendations 171. Introduction 332. Scope and Objectives 393. Methodology 434. Definition and Classification of Eating Disorders 475. Prevention of Eating Disorders 556. Detection of Eating Disorders 637. Diagnosis of Eating Disorders 738. Interventions at the Different Levels of Care in the Management of 81Eating Disorders9. Treatment of Eating Disorders 9110. Assessment of Eating Disorders 17911. Prognosis of Eating Disorders 19112. Legal Aspects Concerning Individuals with Eating Disorders in 195Spain13. Detection, Diagnosis and Treatment Strategies for Eating Disorders 20114. Dissemination and Implementation 21515. Recommendations for Future Research 219ANNEXESAnnex 1. Levels of Evidence and Grades of Recommendation 221Annex 2. Clinical Chapters 223Annex 2.1. Spanish version of the SCOFF survey 223Annex 2.2. Spanish version of the EAT-40 224Annex 2.3. Spanish version of the EAT-26 226Annex 2.4. Spanish version of the ChEAT 227Annex 2.5. Spanish version of the BULIT 228Annex 2.6. Spanish version of the BITE 2345CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Annex 2.7. Diagnostic Criteria for Eating Disorders 236Annex 2.8. Spanish version of the EDE-12 semistructuredinterview 242Annex 2.9. Incorrect Ideas about Weight and Health 242Annex 2.10. Description of Proposed Indicators 243Annex 3. Information for Patients with Eating Disorders and theirFamilies247Annex 3.1. Patient Information 247Annex 3.2. Support Associations for Patients withEating Disorders and their Families 252Annex 4. Glossary 253Annex 5. Abbreviations 261Annex 6. Others 267Annex 6.1. Protocols, Recommendations, TherapeuticOrientations and Guidelines for Eating Disorders 267Annex 6.2. Results of the Search, Selection and QualityAssessment of Evidence based on the stages performed 269Annex 6.3. Description of the NICE’S CPG 270Annex 6.4. Description of the AHRQ’S SRSE 272References 2756CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

PresentationHealth care practice is becoming more and more complex due to multiple factors,the most relevant being the exponential increase of scientific information.To ensure that clinical decisions are appropriate, efficient and safe, health careprofessionals must constantly update their knowledge, an objective that entails greatdedication and effort.In the year 2003, the National Health System’s Interterritorial Council created theHealth Guide (GuíaSalud) project, which aims ultimately to improve evidence-basedclinical decision-making by means of training activities and the configuration of aClinical Practice Guidelines (CPG) register in the NHS. Since then, the Health Guideproject has assessed dozens of CPGs in accordance with explicit criteria generated by itsscientific committee, registered these CPGs and disseminated them throughout theInternet. In early 2006, the Directorate General of the National Health System QualityAgency elaborated the Quality Plan for the National Health System, a plan thatencompasses twelve strategies. The objective of this Plan is to increase cohesion of theNHS and aid in guaranteeing maximum quality health care to all citizens, regardless oftheir place of residence. As part of the plan, the development of eight CPGs onprevalent pathologies related with health strategies was assigned to different agenciesand experts groups. This guide on eating disorders is the result of this assignment.Additionally, the establishment of a common CPG development methodology forthe NHS was assigned to CPG experts groups in our country, resulting in a collectiveeffort of consensus and coordination amongst them.In 2007, the Health Guide project was renovated by creating the Clinical PracticeGuideline Library. This project thoroughly covers the elaboration of CPGs and includesother services and products of evidence-based medicine. It also aims to favour theimplementation and assessment of the use of CPGs in the National Health System.Eating disorders, anorexia nervosa and bulimia nervosa, as well as other similarclinical pictures, are disorders of multifactorial ethiopathogeny that have been a greatchallenge for public health care in the last decades. Sociocultural factors that can lead toeating disorders, as well as the serious physical, social and psychological sequelae thatthese disorders entail have caused great social alarm. Eating disorders are diseases thatnot only involve the affected individual, but also the family and closest environment,and even health care and education professionals who are directly or indirectly involved,and who have no access to guides to address these disorders successfully.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS7

This CPG aims to provide the population and health care and education professionalswith a useful instrument to address the most basic aspects of the disease, especially thoseconcerning prevention and treatment. Understanding and assessing these diseases,identifying them and assessing their risk potential, as well as presenting therapeuticobjectives, and deciding on the best site for treatment and providing help to families, aretasks that can be tackled from different professional settings with an undeniable benefitfor patients and family members. Such is the role that this evidence-based guide aims toexercise, and which is the result of the work performed by a group of professionalsinvolved in the field of eating disorders and experts on CPG methodology.This CPG has been revised by Spanish eating disorders experts and is endorsed bySpanish patient associations and scientific societies involved in the management of thesepatients.Pablo RiveroGeneral DirectorQuality Agency of the National Health SystemCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS8

Authorship and CollaborationsEating Disorders CPG Working GroupFrancisco J. Arrufat, psychiatrist, Consorci Hospitalari de Vic Hospital (Barcelona)Georgina Badia, psychologist, Hospital de Santa Maria (Lérida)Dolors Benítez, research support technician, CAHTA (Barcelona)Lidia Cuesta, psychiatrist, Hospital Mútua de Terrassa (Barcelona)Lourdes Duño, psychiatrist, Hospital del Mar (Barcelona)Maria-Dolors Estrada, preventive physician and Public Health, CAHTA (Barcelona)CIBER of Epidemiology and Public Health (CIBERESP)Fernando Fernández, clinical psychologist, Hospital of Bellvitge,Hospitalet de Llobregat (Barcelona)Joan Franch, psychiatrist, Institut Pere Mata, Reus (Tarragona)Cristina Lombardia, psychiatrist, Parc Hospitalari Martí Julià,Health Care Institute, Salt (Gerona)Santiago Peruzzi, psychiatrist, Sant Joan de Déu Hospital,Esplugues de Llobregat (Barcelona)Josefa Puig, nurse, Hospital Clínic i Provincial de Barcelona (Barcelona)Maria Graciela Rodríguez, clinical and biochemical analyst, CAHTA (Barcelona)Jaume Serra, physician, nutritionist and dietician, Department of Health ofCatalonia(Barcelona)José Antonio Soriano, psychiatrist, Hospital de la Santa Creu i Sant Pau (Barcelona)Gloria Trafach, clinical psychologist, Inastitut d’Assistència Sanitària, Salt (Gerona)Vicente Turón, psychiatrist, Department of Health of Catalonia (Barcelona)Marta Voltas, attorney, Fundación Imagen y Autoestima (Barcelona)CoordinationTechnical CoordinatorMaria-Dolors Estrada, preventive physician and Public Health, CAHTA (Barcelona)CIBER of Epidemiology and Public Health (CIBERESP)Clinical CoordinatorVicente Turón, psychiatrist, Departament of Health of Catalonia (Barcelona)CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS9

External Review of Patient InformationAssociation in Defense of Anorexia Nerviosa and Bulimia Management (ADANER)Spanish Federation of Support Associations for Anorexia y Bulimia(FEACAB)Collaborating societies, associations or federationsThis CPG is endorsed by the following organizations:Luis Beato, Spanish Association for the Study of Eating Disorders (AEETCA)AEETCA is the only scientific society specifically dedicated to eating disordersRosa Calvo, General Council of the Spanish PsychologistAssociationJavier García Campayo, Spanish Society of PsychosomaticsLourdes Carrillo, Spanish Society of Family and CommunityMedicine (SemFYC) (Barcelona)Dolors Colom, General Council of Social WorkersMaría Diéguez, Spanish Neuropsychiatry AssociationAlberto Fernández de Sanmamed, General Council of Spanish Social Educator AssociationsCarlos Iglesias, Spanish Society of Dietetics and Food SciencesPilar Matía, Spanish Society of Endocrinology and NutritionAlberto Miján, Spanish Society of Internal MedicineJosé Manuel Moreno, Spanish Pediatrics AssociationRosa Morros, Spanish Society of Clinical PharmacologyVicente Oros, Spanish Society of Primary Care PhysiciansNúria Parera, Spanish Society of Gynaecology and ObstetricsBelén Sanz-Aránguez, Spanish Society of Psychiatry and Spanish Society ofBiological PsychiatryIngrid Thelen, National Association of Mental Health NursingM. Alfonso Villa, Spanish Odontologist and Stomatologist AssociationDeclaration of Interests:All members of the working group, as well as the individuals who have collaborated in thedevelopment of this guide (experts on eating disorders, representatives from differentassociations, scientific societies, federations and external reviewers), have carried out thedeclaration of conflict of interests by completing a form designed to this end.None of the participants have declared having a conflict of interest related with eatingdisorders.This guide is editorially independent from the funding organisation.11CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Key QuestionsDefinition and Classification of Eating Disorders1. How are eating disorders defined and classified? What are the shared and specific clinicalfeatures of each type?2. Ethiopathogeny of eating disorders: What are the main risk factors?3. What are the most frequent co morbidities of eating disorders?Prevention of Eating Disorders4. What is the efficacy of primary care interventions in avoiding eating disorders? Are there anynegative effects?Detection of Eating Disorders5. What screening instruments are useful to identify cases of eating disorders?Diagnosis of Eating Disorders6. What clinical criteria are useful to diagnose eating disorders?7. How are eating disorders diagnosed?8. What is the differential diagnosis of eating disorders?Interventions at the Different Levels of Care in the Management of EatingDisorders9. What are the primary care (PC) and specialised care interventions for eating disorders?Other resources?10. In eating disorders, what clinical criteria may be useful to assess referral amongst the healthcare resources available in the NHS?11. In eating disorders, what clinical criteria may be useful to assess inpatient care (completehospitalisation) in the healthcare resources available in the NHS?12. In eating disorders, what clinical criteria may be useful to assess discharge in the healthcareresources available in the NHS?Treatment of Eating Disorders13. What is the efficacy and safety of re-nutrition in patients with eating disorders?12CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

14. What is the efficacy and safety of nutritional counselling in patients with eating disorders?15. What is the efficacy and safety of cognitive-behavioural therapy in patients with eatingdisorders?16. What is the efficacy and safety of self-help and guided self-help in patients with eatingdisorders?17. What is the efficacy and safety of interpersonal therapy in patients with eating disorders?18. What is the efficacy and safety of family therapy (systemic or not) in patients with eatingdisorders?19. What is the efficacy and safety of psychodynamic therapy in patients with eating disorders?20. What is the efficacy and safety of behavioural therapy in patients with eating disorders?21. What is the efficacy and safety of antidepressants in patients with eating disorders?22. What is the efficacy and safety of antipsychotic drugs in patients with eating disorders?23. What is the efficacy and safety of appetite stimulants in patients with anorexia nervosa(AN)?24. What is the efficacy and safety of opioid antagonists in patients with eating disorders?25. What is the efficacy and safety of other psychoactive drugs in patients with eatingdisorders?26. What is the efficacy and safety of combined interventions in patients with eating disorders?27. What is the treatment for eating disorders that occur with comorbidities?28. How are chronic cases of eating disorders treated?29. What is the treatment for eating disorders in special situations such as pregnancy and delivery?Assessment of Eating Disorders30. What tools are useful to assess the symptoms and behaviour of eating disorders?31. What tools are useful for the psychopathological assessment of eating disorders?Prognosis of Eating Disorders32. What is the prognosis of eating disorders?13CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

33. Are there prognostic factors for eating disorders?Legal Aspects Concerning Patients with Eating Disorders in Spain34. What legal procedure must be followed when a patient with an eating disorder refuses toreceive treatment?35. Is the informed consent of a minor with an eating disorder legally valid?36. In the case of a minor with an eating disorder, what is the legal solution to the dilemmastemming from the responsibility of confidentiality, respect of autonomy and obligationstowards the minor’s parents or legal guardians?CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS14

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CPG RecommendationsIn this section recommendations are presented following the guide’s structure. Chapters 1,2 and3 of the CPG include an introduction, scope and objectives, and methodology, respectively.Chapter 4 covers eating disorders and Chapter 11 addresses prognosis. All these chapters aredescriptive and thus no recommendations have been formulated for clinical practice. Chapter 5,which covers prevention, is the first to provide recommendations. This section’s abbreviationscan be found at the end.Grade of recommendation: A, B, C o D, depending on whether evidence quality is very high,high, moderate or low. Good clinical practice: recommendation based on the working group’s consensuses.(Please refer to Annex 1).5. Primary Prevention of Eating Disorders (Question 5.1.) 5.1. Sample, format and design characteristics of eating disorder preventionprogrammes that have shown greater efficacy should be considered themodel for future programmes. 5.2. In the design of universal eating disorder prevention strategies, it must betaken into account that expected behavioural changes in children andadolescents without these types of problems might differ from those ofhigh-risk populations. 5.3. Messages on measures that indirectly protect individuals from eatingdisorders should be passed on to the family and adolescent: following ahealthy diet and eating at least one meal at home with the family,facilitating communication and improving self-esteem, avoiding familyconversations from compulsively turning to eating and image andavoiding jokes and disapproval regarding the body, weight or eatingmanner of children and adolescents.6. Detection of Eating Disorders (Question 6.1.)D 6.1. Target groups for screening should include young people with low bodymass index (BMI) compared to age-based reference values, patientsconsulting with weight concerns without being overweight or people whoare overweight, women with menstrual disorders or amenorrhoea, patientswith gastrointestinal symptoms, patients with signs of starvation orrepeated vomiting, and children with delayed or stunted growth, children,adolescents and young adults who perform sports that entail a risk ofdeveloping an eating disorder (athletics, dance, synchronised swimming,etc.).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS16

D 6.2. In anorexia nervosa (AN), weight and BMI are not considered the onlyindicators of physical risk.D 6.3. Early detection and intervention in individuals presenting weight loss areimportant to prevent severe emaciation.D 6.4. In the case of suspected AN, attention should be paid to overall clinicalassessment (repeated over time), including rate of weight loss, growthcurve in children, objective physical signs and appropriate laboratorytests. 6.5. It is recommended to use questionnaires adapted and validated in theSpanish population for the detection of eating disorder cases (screening).The use of the following tools is recommended:Eating disorders in general: SCOFF (for individuals aged 11 years andover)AN: EAT-40, EAT-26 and ChEAT (the latter for individuals aged between8 and 12 years)Bulimia nervosa (BN): BULIT, BULIT-R and BITE (the three forindividuals aged 12-13 years and over) 6.6. Adequate training of PC physicians is considered essential for earlydetection and diagnosis of eating disorders to ensure prompt treatment orreferral, when deemed necessary. 6.7. Due to the low frequency of visits during childhood and adolescence, it isrecommended to take advantage of any opportunity to providecomprehensive management and to detect eating disorder risk habits andcases. Eating disorder risk behaviour, such as repeated vomiting, can bedetected at dental check-ups. 6.8. When interviewing a patient with a suspected eating disorder, especiallyif the suspected disorder is AN, it is important to take into account thepatient’s lack of awareness of the disease, the tendency to deny thedisorder and the scarce motivation to change, these reactions being morepronounced in earlier stages of the disease. 6.9. It is recommended that different groups of professionals (teachers, schoolpsychologists, chemists, nutritionists and dieticians, social workers, etc.)who may be in contact with at-risk population have adequate training andbe able to act as eating disorder detection agents.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS17

7. Diagnosis of Eating Disorders (Questions 7.1.-7.3.) 7.1. It is recommended to follow the WHO’s (ICD-10) and the APA’s (DSM-IV o DSM-IV-TR) diagnostic criteria.D 7.2.1. Health care professionals should acknowledge that many patients witheating disorders are ambivalent regarding treatment due to the demandsand challenges it entails.D 7.2.2. Patients and, when deemed necessary, carers should be provided withinformation and education regarding the nature, course and treatment ofeating disorders.D 7.2.3. Families and carers may be informed of existing eating disorderassociations and support groups. 7.2.4. It is recommended that the diagnosis of eating disorders includeanamnesis, physical and psychopathological examinations andcomplementary explorations. 7.2.5. Diagnostic confirmation and therapeutic implications should be in thehands of psychiatrists and clinical psychologists.8. Interventions at the Different Levels of Care (Questions 8.1.-8.4.)D 8.1. Individuals with eating disorders should be treated in the appropriate carelevel based on clinical criteria: outpatient care, day care (day hospital) andinpatient care (general or psychiatric hospital).D 8.2. Health care professionals without specialist experience in eatingdisorders or who are faced with uncertain situations should seek theadvice of a trained specialist when emergency inpatient care is deemedthe most appropriate option for a patient with an eating disorder.D 8.3. The majority of patients with BN can be treated on an outpatient basis.Inpatient care is indicated when there is risk of suicide, self-inflictedinjuries and serious physical complications.D 8.4. Health care professionals should assess patients with eating disorders andosteoporosis and advise them to refrain from performing physicalactivities that may significantly increase the risk of fracture.D 8.5. The paediatrician and the family physician must be in charge of themanagement of eating disorders in children and adolescents. Growth anddevelopment must be closely monitored.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS18

D 8.6. Primary care centres should offer monitoring and management ofphysical complications to patients with chronic AN and repeatedtherapeutic failures who do not wish to be treated by mental healthservices.D 8.7. Family members, especially siblings, should be included in theindividualized treatment plan (ITP) of children and adolescents witheating disorders. The most common interventions involve sharing ofinformation, advice on behavioural management of eating disorders andimproving communication skills. The patient’s motivation to changeshould be promoted by means of family intervention.D 8.8. Where inpatient care is required, it should be carried out within areasonable distance to the patient’s home to enable the involvement ofrelatives and carers in treatment, to enable the patient to maintain socialand occupational links and to prevent difficulties between care levels.This is particularly important in the treatment of children and adolescentsD 8.9. Patients with AN whose disorder has not improved with outpatienttreatment must be referred to day patient treatment or inpatient treatment.For those who present a high risk of suicide or serious self-inflictedinjuries, inpatient management is indicated.D 8.10. Inpatient treatment should be considered for patients with AN whosedisorder is associated with high or moderate risk due to common disease orphysical complications of AN.D 8.11. Patients with AN who require inpatient treatment should be admitted to acentre that ensures adequate re-nutrition, avoiding the re-feedingsyndrome, with close physical monitoring (especially in the first fewdays), along with the appropriate psychological intervention.D 8.12. The family physician and paediatrician should take charge of theassessment and initial intervention of patients with eating disorders whoattend primary care.D 8.13. When management is shared between primary and specialised care, thereshould be close collaboration between health care professionals, patientsand relatives and carers. 8.14. Patients with confirmed diagnosis or clear suspicion of an eating disorderwill be referred to different health care resources based on clinical andage criteria.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS19

8.15. Referral to adult or children mental health centres (CSMA/CSMIJ) by thefamily physician or paediatrician should consist of integrated care withshared responsibilities. 8.16. Cases referred to adult or children mental health centres (CSMA/CSMIJ)still require different levels to work together and short- and mid-termmonitoring of patients, to avoid complications, recurrences and the onsetof emotional disorders, and to detect changes in the patient’senvironment that could influence the disease. 8.17. The need to prescribe oestrogen treatment to prevent osteoporosis in girlsand adolescents with AN should be carefully assessed, given that thismedication can hide the presence of amenorrhoea. 8.18. In childhood, specific eating disorder treatment programmes designed forthese ages will be required.9. Treatment of Eating Disorders (Questions 9.1.-9.20.)Medical Measures (Re-nutrition and Nutritional Counselling)Re-nutrition (Question 9.1.)Anorexia nervosaD 9.1.1.1. A physical exploration and in some cases oral multivitamin and/ormineral supplements are recommended, both in outpatient and inpatientcare, for patients with AN who are in the stage of body weightrestoration.D 9.1.1.2. Total parenteral nutrition should not be used in patients with AN unlessthe patient refuses nasogastric feeding and/or when there isgastrointestinal dysfunction. 9.1.1.3. Enteral or parenteral re-nutrition must be applied using strict medicalcriteria and its duration will depend on when the patient is able to resumeoral feeding.General Recommendations on Medical Measures (GM) for Eating Disorders(Questions 9.1.-9.2.)Eating Disorders 9.GM.01. Nutritional support for patients with eating disorders will be selectedbased on the patient’s degree of malnutrition and collaboration, andalways with the psychiatrist’s approval.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS20

9.GM.02. Before initiating artificial nutrition the patient’s degree of collaborationmust be assessed and an attempt must always be made to convincehim/her of the benefits of natural feeding. 9.GM.03. In day hospitals, nutritional support for low-weight patients, where anoral diet is insufficient, can be supplemented with artificial nutrition (oralenteral nutrition). To ensure its intake, it must be administered during theday hospital’s hours, providing supplementary energy ranging from 300to 1,000 kcal/day. 9.GM.04. Oral nutritional support in eating disorder inpatients is deemed adequate(favourable progress) when a ponderal gain greater than 0.5 kg per weekis produced, with up to 1 kg increments being the usual during thatperiod. Sometimes, when the patient with moderate malnutrition resistsresuming normal feeding, the diet can be reduced by 500-700 kcal and besupplemented by complementary oral enteral nutrition in the sameamount, which must be administered after meals and not instead ofmeals. 9.GM.05. In the case of severe malnutrition, extreme starvation, poor progress orlack of cooperation of the patient in terms of eating, artificial nutritiontreatment is indicated. If possible, an oral diet with or without oralenteral nutrition is always the first step, followed by a 3 to 6 day periodto assess the degree of collaboration and medical-nutritional evolution. 9.GM.06. Regarding estimated energetic requirements, it is recommended thatcaloric needs at the beginning always be below the usual, that realweight, as opposed to ideal weight, is used to make the estimation andthat in cases of severe malnutrition energetic requirements be 25 to 30kcal/kg real weight or total kcal not higher than 1,000/day.Anorexia nervosaD 9.GM.1. In feeding guidelines for children and adolescents with anorexiaNervosa, carers should be included in any dietary information, educationand meal planning.D 9.GM.2. Feeding against the will of the patient should be used as a last resort inthe management of AN.D 9.GM.3. Feeding against the will of the patient is an intervention that must beperformed by experts in the management of eating disorders and relatedclinical complications.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS21

D 9.GM.4. Legal requirements must be taken into account and complied with whendeciding whether to feed a patient against his/her will.D 9.GM.5. Health care professionals must be careful with the healthy weightrestoration process in children and adolescents with AN, administeringthe nutrients and energy required by providing an adequate diet in orderto promote normal growth and development.Bulimia nervosaD 9.GM.6. Patients with BN who frequently vomit and abuse laxatives can developabnormalities in electrolyte balance.D 9.GM.7. When electrolyte imbalance is detected, in most cases elimination of thebehaviour that caused it is sufficient to correct the problem. In a smallnumber of cases, oral administration of electrolytes whose plasmaticlevels are insufficient is necessary to restore normal levels, except incases involving gastrointestinal absorption.D 9.GM.8. In the case of laxative misuse, patients with BN must be advised on howto decrease and stop abuse. This process must be carried out gradually.Patients must also be informed that the use of laxatives does not decreasenutrient absorption.D 9.GM.9. Patients who vomit habitually must have regular dental check-ups and beprovided with dental hygiene advice.Psychological Therapies for Eating DisordersCognitive-Behavioural therapy (Question 9.3.)Bulimia nervosaA9.3.2.1.1. CBT-BN is a specifically adapted form of CBT and it is recommended that16 to 20 sessions are performed over 4 or 5 months of treatment.B 9.3.2.1.2Patients with BN who do not respond to or refuse to receive CBTtreatment may be offered alternative psychological treatment.D9.3.2.1.3.Adolescents with BN can be treated with CBT adapted to their age, levelof development, and, if appropriate, the family’s intervention can beincorporated.22CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Binge-Eating DisorderA 9.3.3.1. A specifically adapted form of CBT can be offered to adults with bingeeatingdisorder (BED).Self-Help (guided or not) (Question 9.4.)Bulimia nervosaB 9.4.1.1.1. A possible first step in BN treatment is initiating a SH programme(guided or not).B 9.4.1.1.2. SH (guided or not) is sufficient only in a small number of patients withBN.Interpersonal Therapy (Question 9.5.)Bulimia nervosaB 9.5.2.1. IPT should be considered an alternative to CBT although patientsshould be informed that it requires 8 to 12 months to achieve resultssimilar to those obtained with CBT.Binge-Eating DisorderB 9.5.3.1. IPT-BED can be offered to patients with persistent BED.Family Therapy (systemic or not) (Question 9.6)Anorexia nervosaB 9.6.1.1.1. FT is indicated in children and adolescents with AN.D 9.6.1.1.2. Family members of children with AN and siblings and family membersof adolescents with AN can be included in treatment, taking part inimproving communication, supporting behavioural treatment and sharingtherapeutic information.D 9.6.1.1.3. Children and adolescents with AN can be offered individualappointments with health care professionals, separate from those inwhich the family is involved.D 9.6.1.1.4. The effects of AN on siblings and other family members justifies theirinvolvement in treatment.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS23

General Recommendations for Psychological Therapy (GP) in EatingDisorders (GP) (Questions 9.3.-9.8.)Anorexia nervosaD 9.GP.1. The psychological therapies to be assessed for eating disorders are: CBT,SFT, IPT, PDT and BT.D 9.GP.2. In the case of patients who require special care, the selection of thepsychological treatment model that will be offered is even moreimportant.D 9.GP.3. The objective of psychological treatment is to reduce risk, to encourageweight gain by means of a healthy diet, to reduce other symptoms relatedwith eating disorders and to facilitate physical and psychologicalrecovery.D 9.GP.4. Most psychological treatments for patients with AN can be performed onan outpatient basis (with physical monitoring) by professionalsspecialised in eating disorders.D 9.GP.5. The duration of psychological treatment should be of at least 6 monthswhen performed on an outpatient basis (with physical monitoring) and 12months for inpatients.D 9.GP.6. For patients with AN who have undergone outpatient psychologicaltherapy but have not improved or have deteriorated, the indication ofmore intensive treatments (combined individual and family therapy, dayor inpatient care) must be considered.D 9.GP.7. For inpatients with AN, a treatment programme aimed at suppressingsymptoms and achieving normal weight should be established. Adequatephysical monitoring is important during renutrition.D 9.GP.8. Psychological treatments must be aimed at modifying behaviouralattitudes, attitudes related to weight and body shape and the fear ofgaining weight.D 9.GP.9. The use of excessively rigid behaviour modification programmes is notrecommended for inpatients with AN.D 9.GP.10. Following hospital discharge, patients with AN should be offeredoutpatient care that includes monitoring of normal weight restoration andpsychological intervention that focuses on eating behaviour, attitudes toweight and shape and the fear of social response regarding weight gain,along with regular physical and psychological follow-up. Follow-upduration must be of at least 12 months.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS24

D 9.GP.11. In children and adolescents with AN who require inpatient treatment andurgent weight restoration, age-related educational and social needsshould be taken into account.Binge-Eating DisorderA 9.GP.12. Patients must be informed that all psychological treatments have alimited effect on body weight.B 9.GP.13. A possible first step in the treatment of patients with BED is to encouragethem to follow a SH programme (guided or not).B 9.GP.14. Health care professionals can consider providing BED patients with SHprogrammes (guided or not) that may yield positive results. However,this treatment is only effective in a limited number of patients with BED.D 9.GP.15. If there is a lack of evidence to guide the care of patients with EDNOS orBED, health care professionals are recommended to follow the eatingdisorder treatment that most resembles the eating disorder the patientpresents.D 9.GP.16. When psychological treatments are performed on patients with BED, itmay be necessary in some cases to treat comorbid obesity.D 9.GP.17. Adolescents with BED must be provided with psychological treatmentsadapted to their developmental stage.Pharmacological Treatment of Eating DisordersAntidepressants (Questions 9.9.)Bulimia nervosaB 9.9.2.1.1. Patients should be informed that antidepressant treatment can reduce thefrequency of binge-eating and purging episodes but effects are notimmediate.B 9.9.2.1.2. In the treatment of BN, pharmacological treatments other thanantidepressants are not recommended.D 9.9.2.1.3.D 9.9.2.1.4.The dose of fluoxetine used in patients with BN is greater than the doseused for treating depression (60 mg/day).Amongst SSRI antidepressants, fluoxetine is the first-choice drug fortreatment of BN, in terms of acceptability, tolerability and symptomreduction.25CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Binge-Eating DisorderB 9.9.3.1.1. SSRI antidepressant treatment can be offered to a patient with BED,regardless of whether he/she follows a guided SH programme or not.B 9.9.3.1.2. Patients must be informed that SSRI antidepressant treatment can reducethe frequency of binge-eating, but the duration of long-term effects isunknown. Antidepressant treatment may be beneficial for a smallnumber of patients.General Recommendations for Pharmacological Treatment (GPH) of EatingDisorders (Questions 9.9.-9.15.)Anorexia nervosaD 9.GPH1. Pharmacological treatment is not recommended as the only primarytreatment for patients with AN.D 9.GPH.2. Caution should be exercised when prescribing pharmacological treatmentfor patients with AN who have associated comorbidities such asobsessive-compulsive disorder (OCD) or depression.D 9.GPH.3. Given the risk of heart complications presented by patients with AN,prescription of drugs whose side effects may affect cardiac function mustbe avoided.D 9.GPH.4. If drugs with adverse cardiovascular effects are administered, ECGmonitoring of patients should be carried out.D 9.GPH.5. All patients with AN must be warned of the adverse effects ofpharmacological treatments.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS26

Binge-Eating DisorderD 9.GPH.6. In the absence of evidence to guide the management of BED, it isrecommended that the clinician treat the patient based on the eatingproblem that most closely resembles the patient’s eating disorderaccording to BN or AN guides.Treatment of Eating Disorders in the Presence of Comorbidities (Question 9.18)Eating Disorders with Organic DisordersD 9.18.1. Treatment of clinical and subclinical cases of eating disorders in patientswith diabetes mellitus (DM) is essential given the increased risk in thisgroup.D 9.18.2. Patients with Type 1 DM and an eating disorder must be monitored dueto the high risk of developing retinopathy and other complications.D 9.18.3. Young people with type 1 DM and poor adherence to antidiabetictreatment should be assessed for the probable presence of an eatingdisorder.Treatment of Chronic Eating Disorders (Question 9.19.) 9.19.1. The health care professional in charge of the management of chroniceating disorder cases should inform the patient on the possibility ofrecovery and advise him/her to see the specialist regularly regardless ofthe number of years elapsed and previous therapeutic failures. 9.19.2. It is necessary to have access to health care resources that are able toprovide long-term treatments and follow-up on the evolution of chroniceating disorder cases, as well as to have social support to decrease futuredisability.Treatment of Eating Disorders in Special Cases (Question 9.20.)D 9.20.1. Pregnant patients with AN, whether it is the first episode or a relapse,require intensive prenatal care with adequate nutrition and follow-up offoetal development.D 9.20.2. Pregnant women with eating disorders require careful follow-upthroughout pregnancy and the postpartum period.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS27

10. Assessment of Eating Disorders (Questions 10.1.-10.2.)D 10.1.1. Assessment of patients with eating disorders should be comprehensiveand include physical, psychological and social aspects, as well as acomplete assessment of risk to self.D 10.1.2. The therapeutic process modifies the level of risk for the mental andphysical health of patients with eating disorders, and thus should bemonitored throughout treatment.D 10.1.3. Throughout treatment, health care professionals who evaluate childrenand adolescents with eating disorders should be alert to possibleindicators of abuse (emotional, physical and sexual) to ensure an earlyresponse to this problem.D 10.1.4. Health care professionals who work with children and adolescents witheating disorders should familiarise themselves with national CPGs andcurrent legislation regarding confidentiality. 10.1.5. It is recommended to use questionnaires adapted and validated in theSpanish population in the assessment of eating disorders.At present, the following specific instruments for eating disorders arerecommended: EAT, EDI, BULIT, BITE, SCOFF, ACTA and ABOS(the selection of the version should be based on the patient’s age andother application criteria).To assess aspects related with eating disorders, the followingquestionnaires are recommended: BSQ, BIA, BAT, BES and CIMEC(the selection of the version should be based on age and other applicationcriteria). 10.2. The use of questionnaires adapted and validated in the Spanishpopulation is recommended for the psychopathological assessment ofeating disorders. At present, the following instruments forpsychopathological assessment of eating disorders are suggested (versionselection based on patient’s age and other application criteria):Impulsiveness: BIS-11Anxiety: STAI, HARS, CETADepression: BDI, HAM-D, CDIPersonality: MCMI-III, MACI, TCI-R, IPDEObsessiveness: Y-BOCSCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS28

11. Prognosis of Eating Disorders (chapter without recommendations)12. Legal aspects concerning patients with eating disorders in Spain(questions 12.1.-12.2.)12.1. The use of the legal route is recommended in cases where the professionaldeems appropriate to safeguard the patient’s health, while upholding his/herright to be listened to and properly informed on the process and medical andlegal measures that will be applied. Clearly conveying the procedure is not onlyrespectful to the right to information, but can also facilitate the cooperation andmotivation of the patient and his/her environment in the procedure of completehospitalisation (According to current legislation).12.2. One of the characteristic symptoms of eating disorders, and especially of AN, isthe lack of awareness of the disease. The disease itself often entails a lack ofsufficient judgement to provide valid and unmarred consent regarding treatmentacceptance and decision. Hence, if a minor presenting AN and serious healthrisks refuses treatment, the use of appropriate legal and judicial routes shouldbe employed. (According to current legislation).12.3. The necessary balance between different clashing rights requires theprofessional to observe and interpret the best solution in each case. However, itis always important to inform and listen carefully to both parties in order forthem to understand the relationship between safeguarding health and thephysician’s decision. (According to current legislation).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS29

Abbreviations, Clinical Questions and Recommendations. (The complete list ofabbreviations can be found in Annex 5)ABOS: Anorectic Behaviour Observation Scale for parents/spouseACTA: Attitude Towards Change in Eating DisordersAN: Anorexia nervosaAPA: American Psychiatric AssociationBAT: Body Attitude TestBED: Binge-Eating DisorderBDI or Beck: Beck Depression InventoryBES: Body Esteem ScaleBIA: Body Image AssessmentBIS-11: Barrat Impulsivity ScaleBITE: Bulimic Investigation Test of EdinburghBN: Bulimia nervosaBMI: Body Mass IndexBPD Borderline Personality DisorderBSQ: Body Shape QuestionnaireBT: Behavioural TherapyBULIT: Bulimia testBULIT-R: Revised version of BULITCBT: Cognitive-behavioural therapyCBT-BN: Cognitive-behavioural therapy for bulimia nervosaCBT-TA: Cognitive-behavioural therapy for binge-eating disorderCDI: Children Depression InventoryCETA: Assessment of anxiety disorders in children and adolescentsChEAT: Children’s Eating Attitude TestCIMEC: Questionnaire on Influences on the Aesthetic Body Model (Body ShapQuestionnaire (BSQ)CPG: Clinical Practice GuidelineDM: Diabetes mellitusDSM-IV-TR: Diagnostic and Statistical Manual of Mental Disorders, fourth edition- revisedtextEAT (EAT-40): Eating Attitude TestEAT-26: Short version of EAT-40ECG: ElectrocardiogramCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS30

ED: Eating disorderEDNOS: Eating disorder not otherwise specified (non-specific ED)EDI: Eating Disorder InventoryFT: Family therapy (non-specific)GPH: General recommendations for pharmacological treatmentsGM: General recommendations for medical measuresGP: General recommendations for psychological therapiesHAM-D: Hamilton Depression ScaleHARS: Hamilton Anxiety ScaleICD-10: International Classification of Diseases, 10th editionIPDE: International Personality Disorder ExaminationIPT: Interpersonal therapyIPT-BED: Interpersonal therapy for binge-eating disorderITP: Individualized Treatment PlanKcal.: KilocalorieKg: KilogramMHC: Mental Health CentreMHCFA Mental Health Centre for AdultsMGCFCA Mental Health Centre for Children and AdolescentsMACI: Millon Adolescent Clinical InventoryMCMI-III: Millon Multiaxial Clinical Inventory-IIINHS: National Health SystemOCD: Obsessive-Compulsive DisorderPDT: Psychodynamic TherapyPC: Primary careSCOFF: Sick, Control, One, Fat, Food questionnaireSH: Self-helpSSRI: Selective Serotonin Reuptake InhibitorSTAI: State-Trait Anxiety InventoryTCI-R: Temperament and Character Inventory-revisedY-BOCS: Yale-Brown obsessive-compulsive scale31CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS32

1. IntroductionBackgroundThe development of the evidence-based clinical practice guideline elaboration Programmefor the NHS is being carried out 2ithin the framework of the development of the Quality Plan ofthe Ministry of Health and Consumer Affairs (MSC), through the National Health System(NHS)’s Quality Agency.In the initial phase of this Programme (2006), the development of eight CPGs has beenprioritised. A collaboration agreement has been established between the ISCIII and healthtechnology assessment agencies and units and the Iberoamerican Cochrane Centre. The HealthSciences Institute of Aragón is in charge of the Programme’s coordination activities.In the bilateral agreement between the CAHTA of Catalonia and the ISCIII it was agreed todevelop a CPG for eating disorders: anorexia nervosa (AN), bulimia nervosa (BN) and atypicalor unspecified eating disorders (EDNOS), based on the best scientific evidence available, whichwould address the most important areas for the NHS, in a coordinated manner and with sharedmethodology which would be determined by a group of NHS professionals experienced in CPGdevelopment. These professionals have comprised the methodological group and the panel ofcollaborators of the CPG development programme (1) .JustificationIn the last decades, eating disorders have gained increasing sociosanitary relevance due totheir severity, complexity and difficulty in establishing a diagnosis and specific treatment.Eating disorders are pathologies of multifactorial ethiology where genetic, biological,personality, family and sociocultural factors converge, affecting mainly children, adolescentsand young adults.There are is no data available in Spain that analyses the economic burden of eatingdisorder treatments nor studies that assess the cost-effectiveness of different treatments.However, different studies conducted in countries of the European Union 2-7 indicate that directcosts (diagnosis, treatment and monitoring or follow-up) and especially indirect costs (economiclosses derived from the disease that impact the patient and his/her social setting) entail a higheconomic burden and considerably decrease the quality of life of patients with eating disorders.According to a German study that was carried out in 2002, in the case of AN, averagehospitalisation cost is 3.5 times higher than the general hospitalisation average 4 .(1)N= 2,188 AN discharges, recorded during 2003 and 2004 in 156 health areas of 15 autonomous communities.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS33

In 2002, Gowers SG, et al. 8 published the results of a survey conducted in 12 countries thatwere participating in the European project COST Action B6, which aimed to explore consensusand differences in the therapeutic approaches indicated for adolescents with AN (severaldifferent Spanish hospitals participated in this project). Results demonstrated significantagreement between the interviewed countries regarding the need to offer a wide array of servicesat the different levels of care. However, considerable differences were detected in terms ofstrategies, especially in hospital admission criteria, use of day centres/day hospitals, etc.In the case of AN 1 , according to the Atlas of Variations in medical practice of the NHS,where the variability in admissions into acute care public or publicly funded 9 hospitals, aredescribed and mapped, a low hospitalisation incidence is observed in AN with, 0.32 admissionsper 10,000 inhabitants and year. Hospitalisation rates for AN ranged between 0.08 –practicallynil- and 1.47 admissions per 10,000 inhabitants and year. In terms of the weighted variationcoefficient, the figures confirmed the wide variation among the different health areas in 70% ofAN cases. After consideration of the variation randomised effect, the systematic component ofvariation of the health areas included in the percentiles 5 to 95 shows high variability (SCV 5-95 =0,26). The ample variation found may be related either to demand factors (different morbidity,socio-economic differences of the cities and towns) or to offer factors (practice style, healthcareresources, different policies for the development of mental care procedures, etc. The variabilityobserved in hospitalisation rates among Spanish provinces is significant and accounts for a 40%of the variability in hospitalisation rates in cases of AN. Upon multilevel analysis, provinciallevel accounts for a larger variance proportion than in the region (regional level), reinforcing thehypothesis that the different provincial development of psychiatric models and services is behindthe variations found. The remaining studied factors (age, gender, available income, educationallevel, predisposition to hospitalisation) do not appear to exert an influence upon the variabilityobserved in hospitalisation rates in AN, save for the recorded unemployment that works in theopposite way: in areas with more recorded unemployment, the probability of hospitalisation islower. No data are available for BN or eating disorder not otherwise specified (EDNOS-atypicaleating disorders).Different governmental Spanish and foreign institutions have published guides,recommendations and protocols on EDs in the last years, of which the following stand out:• Osona (2008) 10 and the Gerona health region (2006) 11 from the Department of Health-CatalanHealth Service• semFYC (prevention activities and health promotion group) (2007) 12 , (2005) 13 .• American Psychiatric Association (2006) 14 .• Action Manual of the Ministry of Health and Consumer Affairs on the scientific evidenceregarding specialised nutritional support (2006) 15 .• General subdirectorate of Mental Health- Health Service of Murcia (2005) 16 .• Official College and Board of Physicians of Barcelona(2005) 17 .• Royal Australian and New Zealand College of Psychiatrists (2004) 18 .• National Health Institute (INSALUD, 2000) 19 , (1995) 20 .CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS34

However, there is a need for a guide adapted to the Spanish population using the bestpossible methodology and based on the best available evidence.Recently, other important actions related with eating disorders have been carried out in ourcontext, such as: NAOS and PAOS programme for the prevention of obesity in children and ahealthy diet; the Social Pact of the Madrid for the prevention of eating disorders; Image andSelf-Esteem Foundation, and pacts between user federations (FEACAB and ADANER) and theMSC.Magnitude of the problemEstimations on the incidence and prevalence of eating disorders vary depending on the studiedpopulation and assessment tools employed. Therefore, in order to compare data from differentnational and international sources it is essential that the study design be the same. The study in“two phases” is the most appropriate methodology for the detection of cases in the community.The first phase consists of screening using self-report symptom questionnaires. In the secondphase, assessment is carried out by means of clinical interviews that are conducted withindividuals who obtained scores above the cut-off point in the screening questionnaire (“at risk”subjects), meaning only a subsample of the total initially screened sample is interviewed.Within the studies that use correct two-phase methodology, very few perform randomsampling of participants who score below the cut-off point of the screening questionnaire tointerviews, which leads to a subestimation of the prevalence of eating disorders by not takingfalse negatives into account 21-23 . An additional problem is the use of different cut-off points inscreening questionnaires.In spite of these methodological difficulties, the increased prevalence of eating disorders issignificant, especially in developed or developing countries, while it is nearly inexistent in thirdworldcountries. Increased prevalence is attributable to increased incidence and duration andchronicity of these clinical pictures.Based on two-phase studies conducted in Spain (Tables 1 and 2) on the highest risk population,women ranging from 12 to 21 years of age, a prevalence of 0.14% to 0.9% is obtained for AN,0.41% to 2.9% for BN and 2.76% to 5.3% in the case of EDNOS. In total, we would be lookingat an eating disorder prevalence of 4.1% to 6.41%. In the case of male adolescents, even thoughthere are fewer studies available, a prevalence of 0% for AN, 0% to 0.36% for BN and 0.18% to0.77% for EDNOS is obtained, with a total prevalence of 0.27% to 0.90% 21-29 .These numbers are similar to those presented in the NICE CPG (2004), where prevalence inof EDNOS, BN and AN in women ranges from 1% to 3.3%, 0.5% to 1.0% and 0.7%,respectively, and also to those in the Systematic Review of Scientific Evidence (SRSE) (2006)which reports prevalence in Western Europe and the United States (0.7% to 3% of EDNOS inthe community, 1% of BN in women and 0.3% of AN in young women).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS35

Several studies on the incidence of eating disorders that have been published in NorthAmerica and Europe present a 5- to 6-fold increase in incidence between 1960 and 1970. In1998, a review presented by Pawluck, et al. on the general population of the United Statesreported that annual incidence of AN was 19 per 100,000 in women and 2 per 100,000 inmales 30 . In the review presented by Hoek in 2003, incidence was 8 cases per 100,000 inhabitantsfor AN and 12 cases per 100,000 inhabitants for BN 32 .In a recent study in the United Kingdom (UK), incidence for AN in 2000 was 4.7 per100,000 inhabitants (95% CI: 3.6 to 5.8) and 4.2 per 100,000 inhabitants in 1993 (95% CI: 3.4 to5.0). In Holland, incidence of AN was 7.7 (95% CI: 5.9 to 10.0) per 100,000 inhabitants/yearbetween 1995-1999 and 7.4 between 1985 and 1989 33 . In Navarra, a population survey in 1,07613-year old girls was used to estimate an eating disorder incidence of 4.8% (95% CI: 2.84 to6.82) in a period of 18 months, corresponding to: 0.3% AN (95% CI: 0.16 to 0.48): 0.3% BN(95% CI: 0.15 to 0.49) and 4.2% EDNOS (95% CI: 2.04 to 6.34) 34 .Incidence was greater in women aged 15 to 19 years: they constitute approximately 40%of identified cases in studies both in the US and Europe 30, 31, 33 . There are very few studies thatreport data on AN in prepubertal children or in adults 31 . There are also scarce studies thatpresent incidence data of AN in men. Of all the aforementioned studies, we can conclude thatincidence is lower than 1 per 100,000 inhabitants/year 33 . All these sources establish an eatingdisorder prevalence ratio of 1 to 9 in males versus women.Table 1. Studies on the prevalence of eating disorders in adolescent females in SpainStudy NAge(years)AN(%)BN(%)EDNOS(%)EDs(%)Madrid, 1997 24Morandé G and Casas J.723 15 0.69 1.24 2.76 4.69Zaragoza, 1998 26Ruiz P et al.2,193 12-18 0.14 0.55 3.83 4.52Navarra, 2000 27Pérez-Gaspar M et al.2,862 12-21 0.31 0.77 3.07 4.15Reus, 2008 29Olesti M et al.551 12-21 0.9 2.9 5.3 9.136CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Table 2. Studies on the prevalence of eating disorders in adolescent males and females in SpainStudyNAge(years)AN(%)BN(%)EDNOS(%)EDs(%)Madrid, 1999 25Morandé G et al.1,314 15 0.00 to 0.69 0.36 to 1.24 0.54 to 2.763.044.700.90Valencia, 2003 21Rojo L et al.544 12-18 0.00 to 0.45 0.00 to 0.41 0.77 to 4.712.915.560.77Ciudad Real, 2005 22Rodríguez-Cano T et al.1,766 12-15 0.00 to 0.17 0.00 to 1.38 0.60 to 4.86Osona (Barcelona), 2006 28Arrufat F2,280 14-16 0.00 to 0.35 0.09 to 0.44 0.18 to 2.70Madrid, 2007 23Peláez MA et al.1,545 12-21 0.00 to 0.33 0.16 to 2.29 0.48 to 2.723.716.410.601.903.490.273.435.340.6437CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS38

2. Scope and ObjectivesTarget PopulationThe CPG is focused on patients aged 8 years and older with the following diagnoses: AN,BN and eating disorders not otherwise specified (EDNOS). EDNOS include: binge-eatingdisorder (BED) and non-specific, incomplete or partial forms that do not satisfy all criteria forAN, BN and BED.Although binge-eating disorder is the standard name, the truth is that several recurrentbinge-eating episodes must take place to establish this diagnosis (amongst other manifestations).This guide refers to this disorder as binge-eating disorder.The CPG also includes treatment of chronic eating disorder patients, refractory totreatment, who can be provided with tertiary prevention of the most serious symptoms andsevere complications.ComorbiditiesThe most frequent comorbidities which may require a different type of care have been includedin the CPG:• Mental: substance abuse, anxiety, obsessive-compulsive, personality, mood and impulsecontrol disorders.• Organic: diabetes mellitus, obesity, malabsorbtion syndromes and thyroid diseases.Special situationsThe approach to be employed in special situations such as pregnancy and delivery is alsoincluded.Clinical settingThe CPG includes management provided in PC and specialised care. PC services are performedin primary care centres (PCC), the first level of access to health care. Patients with eatingdisorders receive specialised care, the second and third levels of access to health care, by meansof inpatient management resources (psychiatric and general hospital), specialised outpatientconsultations (adult and child/adolescent mental health centres/units, day hospitals for day care(partial hospitalisation) (specialised in eating disorders and for other general mental healthdisorders), emergency services and medical services of general hospitals. In general hospitalsthere are specific units specialised in eating disorders that include the three care levels. Othertypes of specific units are included: borderline personality disorder and toxicology units.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS39

Aspects includedThe CPG includes the following aspects of eating disorders: prevention, detection, diagnosis,interventions at the different levels of care, treatment, assessment, prognosis and legal aspects.InterventionsThe CPG includes the following interventions for primary prevention of eating disorders:psychoeducational interventions, media literacy, social and political mobilization and activism(advocacy), dissonance-induction techniques, interventions focused on eliminating or reducingthe risk factors of eating disorders or interventions to make the patient stronger (by developingstress coping skills).Some of the outcome variables of primary prevention interventions are: incidence of eatingdisorders, BMI, internalisation of the thin-ideal, body dissatisfaction, anomalous diet, negativeaffects and eating disorders.The CPG includes the following treatments:• Medical measures: oral nutritional support, nutritional support with artificial nutrition (enteraloral [nasogastric tube] and parenteral intravenous) and nutritional counselling (NC). NCincludes dietary counselling, nutritional counselling and/or nutritional therapy.• Psychological therapies: cognitive-behavioural therapy (CBT), self-help (SH), guided self-help(GSH), interpersonal therapy (IPT), family therapy (systemic [SFT] or unspecified [FT]),psychodynamic therapy (PDT) and behavioural therapy (BT).• Pharmacological treatments: antidepressants, antipsychotics, appetite stimulants, opioidantagonists and other psychoactive drugs (topiramate, lithium and atomoxetine).• Combined interventions (psychological and pharmacological or more than one psychologicalintervention).Clinically important treatment outcome variables according to the working group are: BMI,menstruation, pubertal development, reduction/elimination of binge-eating and purging,restoration of a healthy diet, absence of depression and psychosocial and interpersonalfunctioning. The latter two aspects are described in the questions regarding safety ofinterventions.In some cases, recurrence or relapse results are described in the safety section, along withtreatment withdrawls.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS40

Aspects not included in the CPGThe CPG does not include the following diagnoses related with eating disorders for severalreasons:• Orthorexia. A poorly defined and insufficiently studied syndromic spectrum that consists ofextreme focus on eating healthy and contaminant-free foods. This disorder can be related toobsessive concerns about health, hypochondriac fears of diseases, and, in a certain way, tocultural attitudes linked to diet and food. Though it is true that people with orthorexia maypresent restrictive anomalies in their diets and ponderal losses, they cannot be consideredatypical or incomplete cases of AN.• Vigorexia (muscle dysmorphia). This disorder is characterized by excessive concern aboutobtaining body perfection by performing specific exercises. This extreme preoccupationentails significant dissatisfaction with one’s own body image, excessive exercise, special dietsand foods, to the point of generating dependence, as well as substance abuse 35 . At the momentit remains a vaguely defined disorder related with obsessiveness, perfectionism anddysmorphophobia 36-40 .• Night eating syndrome (nocturnal eaters). People with this disorder experience recurrentepisodes of binge-eating during sleep. It is not defined whether these clinical pictures are dueto an eating disorder or to a primary sleep disorder 41-44 .The CPG does not include patients under the age of 8 and, thus, diagnoses relating to eatingdisorders most common during those ages, such as swallowing phobia, selective eating andrefusal to eat are not included. However, these disorders are not included either when they areobserved in patients aged 8 and older for the following reasons:• Food phobia (simple phobias). In some cases it may be an anxiety-related disorder, while inothers it may be linked to hypochondria (fear of choking, swallowing phobia and death).Therefore, it does not seem to belong to the spectrum of eating disorders.• Selective eating and refusal to eat. Both are eating disorders but lack the complete andcharacteristic symptomatology associated with AN and BN (cognitive disturbances, distortedbody image, purging behaviours, etc).This does not mean that when deciding on primary prevention policies no interventions shouldbe carried out to address these behaviours, which could indeed be precursors of an eatingdisorder.The CPG does not include exclusive interventions for comorbid conditions that may occurwith eating disorders.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS41

ObjectivesMain objectiveTo provide health care professionals responsible for the management of patients with eatingdisorders with a tool that enables them to make the best decisions to address the problems theircare entails.Secondary objectivesa) To help patients with eating disorders by providing them with useful information thatwill aid them in making decisions concerning their disease.b) To inform families and carer on eating disorders and provide them with counselling andadvice so they become actively involved in treatment.c) To implement and develop health care quality indicators that enable the assessment ofthe clinical practice of recommendations presented in this CPG.d) To establish recommendations for research on eating disorders that enable knowledge togrow.e) To address confidentiality and informed consent issues of patients, especially in the caseof minors under the age of 18, and to include legal procedures in the cases of completehospitalisation (inpatient care) and involuntary treatment.Main usersThis CPG is aimed at professionals who are in direct contact with patients with eating disordersor who make decisions regarding the care of these patients (family physicians, paediatricians,psychiatrists, psychologists, nurses, dieticians, endocrinologists, pharmacists, gynaecologists,internal medicine physicians, odontologists, occupational therapists and social workers). It isalso aimed at professionals pertaining to other fields who are in direct contact with patients witheating disorders (education, social services, media, justice).The CPG’s purpose is to serve as a tool for planning the integrated care of patients witheating disorders.The CPG provides eating disorder patients with information that can also be used by familymembers and friends, as well as by the general population.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS42

3. MethodologyThe methodology employed is described in the MSC’s CPG development manual 1 . The stepsfollowed have been:– Creation of the CPG working group comprised of a clinical team, a technical team and twocoordinators (clinical and technical). The clinical team consists of a group of health careprofessionals (psychology, psychiatry, nursing and nutrition and dietetics specialists)involved in the study and treatment of eating disorders and an attorney, who are carryingout their activity in Catalonia and are linked to the Master Plan of Mental Health andAddictions of the Catalan Department of Health, and representatives of Spanish scientificsocieties, associations or federations who are involved in the care of eating disorders. Thetechnical team is composed of CAHTA members who have a wealth of experience andknowledge on the development of evidence-based CPGs and on critical assessment, andresearch support staff. The working group has relied on the participation of a group ofcollaborating experts from all over Spain selected by the clinical coordinator for hisexpertise in the matter, as well as another group of CAHTA members who havecollaborated in some of the following activities: defining the scope, search, documentalmanagement, initial review of literature and internal review. Representatives of thesocieties, associations or federations involved in this project and expert collaborators havetaken part in defining the scope and objectives of the CPG, in the formulation of keyclinical questions and in the review of the guide’s rough draft. The participants’declaration of conflict of interests can be found in the section “Authors andCollaborations”.– Formulation of key clinical questions in the following format: patient / intervention/ comparison / outcome or result (PICO).– The search for scientific evidence was structured in different stages:1) Generic databases, meta-search engines and organizations that compile guidelines(National Guidelines Clearinghouse, National Electronic Library for Health,Tripdatabase, The Cochrane Library, Pubmed/Medline and BMJ Clinical Evidence)were consulted between 2003 and March 2007.2) To complete the search, a manual search was performed for protocols, recommendations,narrative reviews, therapeutic orientations and guides on eating disorders elaborated byorganisations pertaining to the health care administration, scientific societies, hospitalsand other organizations of our setting. Some of these documents have inspired andserved as a model for certain sections of this guide (see Annex 6.1.). This annex alsolists documents created outside of Spain that have been excluded from the selectionprocess due to low quality. However, some have been considered for the developmentof certain aspects of this CPG.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS43

3) To respond to those questions unanswered by the CPGs, SRSE and assessment reports(AR) included or to update them, a search for randomised controlled trials (RCTs) wasperformed in Pubmed/Medline between March 2007 and October 2007.4) The search for CPG/SRSE/AR in Tripdatabase and Pubmed/Medline was also updatedup to October 2007.5) Additional searches were carried out in Pubmed/Medline and Scopus for primaryprevention of eating disorders due to the limited information available in the documentsincluded (until June 2008). The effect of primary prevention interventions for eatingdisorders has been assessed in RCT or in SRSE of RCT.6) A search was also performed for cohort studies and prognosis of eating disorders in theScopus and Psycinfo databases during the period spanning from 2000 to 2008.7) The Ginebrina Foundation was also consulted for Medical Training and Research and thedocuments provided by the working group and the references of the documentsincluded were reviewed.– Selection of Evidence. The most relevant documents were selected by applying predefinedinclusion and exclusion criteria:• Inclusion criteria: guides, SRSE and ARs in certain languages (Spanish, Catalan, French,English and Italian) that dealt with the previously mentioned objectives. Minimumquality criteria were established for the guides, SRSE and ARs: the bibliographic basesconsulted and/or the formulation process of recommendations (ad hoc defined criteria)had to be described.• Exclusion criteria: documents/guides that were not original, unavailable (wrong referenceor electronic address), not directly related with the proposed objectives, already includedin the bibliography of other documents/guides or that didn’t comply with minimumquality criteria.Two independent reviewers examined the titles and/or summaries of the documents identified bythe search strategy. If any of the inclusion criteria were not fulfilled, the document wasexcluded. If criteria were fulfilled, the complete document was requested and evaluated in orderto decide whether it would be included or not. Discrepancies or doubts that arose during theprocess were resolved by consensus of the entire technical team.– Quality assessment of the scientific evidence. Assessment of CPG quality was performed bya trained evaluator using the AGREE 45 instrument. Guides were considered of quality whenthey were classified as Recommended in the overall assessment. For SRSE/ARs and RCT,SIGN’s methodology checklists were applied by an evaluator, following the recommendationsestablished in the MSC’s 1 CPG development manual. Classification of evidence has beencarried out using the SIGN system (See Annex 1).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS44

– Synthesis and analysis of the scientific evidence. Different templates were used forinformation retrieval. Information regarding the main characteristics of the studies wasobtained and then synthesised in evidence tables for a subsequent qualitative analysis. Whenthe SRSE or CPGs reported the results of individual studies, these results were described in thesection “scientific evidence”.In Annex 6.2 results of the CPG’s search, selection and assessment of quality are described. InAnnex 6.3. and Annex 6.4. NICE’s CPG 30 and AHRQ’s SRSE 31 are respectively described,representing the main scientific base on which this guide is founded.– Formulation of recommendations based on formal assessment or on SIGN’s consideredjudgement. The grading of recommendations has been performed using SIGN’s system (SeeAnnex 1). Recommendations pertaining to the NICE CPG have been considered by theworking group and have been classified as: adopted (and, hence, accepted; they have simplybeen translated into Spanish) or adapted (and, hence, modified: changes have been made withthe purpose of contextualising them to our setting). Controversial recommendations or thoselacking in evidence have been resolved by the working group’s consensus. The category ofeach recommendation appears in the chapters.– Description of psychological therapies. Definitions are derived from the NICE 30 guide, fromthe SRSE where they have been assessed and from the working group itself (See Annex 4).– Description of drugs (mechanism of action and approved indications in Spain) included in theCPG. The following websites have been consulted: Spanish Drug Agency (AGEMED)(https://agemed.es) and Vademecum (http://www.vademecum.es). It is recommended to readthe technical chart of each drug before any therapeutic prescription given that the CPG onlyincludes a very brief description of each drug and does not go into depth in terms of schemes,contraindications, etc. (See Annex 4).– Legal aspects. To develop this chapter, aside from reviewing the current legislation in ourcountry, several different articles and reference documents 17, 46-49 have been consulted.– To develop patient information (See Annex 3.1.), a search has been performed for pamphletsand other documents containing information for the patient/carer both in printed and electronicformats. To this end, all documents identified in the websites of three relevant organizations(www.feacab.org, www.itacat.com and www.adaner.org) that comprise the majority ofassociations declared of public use at a national level through their different delegations andsupport groups and the material provided by the clinical coordinator have been reviewed.Following the review of these documents, a content comparison table was elaborated from whichthe table of contents was developed. Once consensus of the final version had been reached bythe working group and collaborating experts, the Association in Defence of Anorexia Nervosaand Bulimia Management (ADANER) and the Spanish Federation of Support Associations forAnorexia (FEACAB), which include most local organisations, carried out an external review,using a specifically designed questionnaire that inquired on the suitability of the informationprovided, the examples used, style and language, etc. Although this information is part of theCPG and must be delivered and explained to the patient/carer by health care professionals, wehope to edit individualised pamphlets that facilitate its dissemination.45CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

– Formulation of research lines. They have been developed from the research lines that areincluded in AHRQ 2006 31 (See chapter 15). G– The external reviewers of the CPG are a group of experts in eating disorders (psychiatry,psychology and genetics specialists) selected for being heads of eating disorder units inSpanish hospitals and/or authors of relevant publications on the matter. Representatives fromcertain organizations who were unable to be a part of the CPG working group for a variety ofreasons also served as external reviewers. The final version of the guide’s text has beenrevised and approved by the group of authors.– The updating of this CPG published in 2009 will be carried out after assessing new evidencethat may arise in the next three years. Any changes made during this time will be reflected inthe electronic format available at the GuíaSalud portal and the CAHTA website. To carry outguideline updating, the methodology proposed in the MSC’s 1 CPG development manual willbe applied.– Resources containing detailed information on the CPG methodological process are available atthe GuíaSalud portal (www.guiasalud.es).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS46

4. Definition and Classification of EatingDisordersKey Questions:4.1. How are eating disorders defined and classified? What are the shared and specificclinical features of each type?4.2. Etiopathogeny of eating disorders: What are the main risk factors?4.3. What are the most frequent comorbidities of eating disorders?4.1. How are eating disorders defined andclassified?What are the shared and specific clinical features ofeach type?Eating disorders are a group of mental disorders characterised by disordered eating behaviourand the development of behaviours aimed at managing weight. These behaviours lead tophysical problems and deteriorated psychosocial functioning of the patient. Currentclassifications of eating disorders include AN, BN and other less specific disorders known asEDNOS (See chapter 7, “Diagnosis”).The first descriptions of AN date back to the 17th century, when Morton determined thatthe origin of this disorder, in contrast to other states of malnutrition, was a disturbance of thenervous system accompanied by sadness and pre-occupation. In the 19th century, it wasdescribed as an individual psychopathological picture similar to the one observed today, thoughit was believed to be a mood disease. Although the history of BN is much younger, the numberof affected patients has been growing significantly in the past few years, possibly due to its lessdramatic evolution and the ease with which affected individuals go undetected.AN is an eating disorder that manifests itself as an uncontrollable desire to be thin,accompanied by the voluntary practice of procedures to achieve this goal: a strict, restrictive dietand purging behaviour (self-induced vomiting, laxative abuse, use of diuretics, etc). Despitegradual weight loss, patients present an extreme fear of becoming obese. They present bodyimage distortion and an extreme pre-occupation with diet, figure and weight, and thus engage infood avoidance behaviour by means of compensatory actions to compensate for what they haveingested (extreme physical hyperactivity, purging behaviour, etc). Patients are not usually awareof the disease or the risks their behaviour entails. Their attention is focused on ponderal loss,leading to deficient nutritional states and ultimately to life-threatening risks. Usually there areprevious personality traits that tend towards conformism, the need for approval,hyperresponsibility, perfectionism and poor response to internal needs.47CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

BN is an eating disorder characterised by binge-eating episodes (voracious anduncontrolled eating), in which a large amount of food is consumed in a short period of time andusually in secret. Affected individuals attempt to counteract the effects of over-eating by meansof self-induced vomiting and/or other purging methods (misuse of laxatives and diuretics, etc.)and physical hyperactivity. These individuals present pathological concern about weight andfigure. BN does not necessarily lead to weight changes. Patients can present normal, low orexcess weight. BN tends to be a hidden disorder given that it goes easily undetected and patientsdeal with feelings of shame and guilt. Patients usually seek help when the problem hasprogressed to advanced stages.EDNOS are usually incomplete AN or BN pictures that do not constitute a completepicture. They are not, however, less serious. EDNOS include disorders such as the frequent useof inappropriate compensatory behaviour (after eating, chewing and spitting out small amountsof food) and recurrent compulsive eating episodes without compensatory behaviour. BED is adisorder that is currently in the study phase to determine if it is a disorder different from otherEDNOS or simply a light form of BN. The main difference with BN is the absence ofcompensatory mechanisms, which eventually lead the patient to inevitably become overweightor obese.What are the shared clinical features of AN and BN?At a psychopathological level, AN and BN share an excessive pre-occupation with image andweight, which reaches irrational extremes in AN (not in BN). At a physical level,malnourishment and its potential complications are always present in AN and possible in thecase of BN. There are also mixtures of anorexic and bulimic behaviour that are hard todifferentiate, although ponderal loss and secondary malnutrition point to AN.What are the specific clinical features of AN?– Refusal to maintain normal body weight or to gain ponderal weight and distortion of bodyimage: patients with AN are focused on their body weight, on the dread of gaining weight orbecoming fat (a fear that is compounded as the patient loses weight) and on the desire to loseweight. An altered body experience is a core factor in the concept of eating disorders.Dissatisfaction with one’s own body image is the main reason for weight loss, especially if itis associated with low self-esteem. It is a phobic fear of becoming fat and losing control overfood. These ideas lead to behaviours aimed at achieving ponderal loss.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS48

– Other psychopathological disturbances: symptoms such as depressive mood, apathy, difficultyconcentrating, anxiety, irritability, social alienation, loss of sexual drive, brooding and/orobsessive rituals regarding food are usually present.– Physiological disturbances: as a consequence of ponderal loss there is malnutrition, leading tosecondary disturbances, especially hormonal and metabolic 72 .– Amenorrhoea (primary or secondary): a characteristic symptom of the disease, it can appear inup to 70% of cases when there is significant ponderal loss. 20% of patients presentamenorrhoea without prior detectable weight loss. This is due to hypogonadotrophichypogonadism originated by a hypothalamic dysfunction that is considered to be primarilyproduced by a reduction of calorie intake and weight loss 73 .– Physical hyperactivity: Is usually present from the beginning of the disease. These individualspresent two types of hyperactivity: deliberate physical exercise aimed at burning calories andlosing weight, which can be practiced alone, presents obsessive characteristics and occurs onlyin a minority of patients, and involuntary hyperactivity secondary to malnutrition, which is anautomatic response that manifests as persistent restlessness similar to that observed inlaboratory animals subjected to hypocaloric intake.What are the specific clinical features of BN?– Loss of control over eating behaviour, which serves to understand recurrent binge-eatingepisodes. During these episodes, patients eat large amounts of food in a short period of time.The duration of these episodes can vary (approximately 2 hours), but is always within a 2-hour period; in fact, eating small amounts of food throughout the day is not considered abinge-eating episode, even though the episode does not have to occur in one place solely (forexample, an individual may begin the episode in a restaurant and end it at home). Overall,even though the types of food eaten during the episode vary, in most cases it is sweets andhigh-calorie foods that are ingested, such as ice-cream or cake; quantity can also vary butmay amount to several kilograms. Binge-eating episodes can occur at any time of the daybut are more frequent at mid-afternoon and onward. They may be triggered by dysphoricmoods, interpersonal difficulties, intense hunger or after restrictive diets or feelings relatedwith weight, body figure or food. Episodes are accompanied by a feeling of losing controland can temporarily reduce dysphoria, but are always followed by feelings of guilt, selfcontemptor depressive mood 74 .– Presence of compensatory mechanisms aimed at avoiding weight gain: 80% to 90% ofpatients engage in self-induced vomiting after the binge-eating episode. The immediateeffect is relief of physical discomfort and decreased fear of gaining weight. The mostfrequent way of self-inducing vomiting is by inserting the hand to trigger the nauseousreflex. With time, it becomes easier to induce vomiting, and may be done by simplycompressing the abdomen. Other mechanisms used to avoid weight gain are the misuse oflaxatives and diuretics, the use of other anorexigenic drugs, excessive exercise or fasting.Both laxatives and diuretics cause dehydration and the resulting feeling of ponderal loss, butwhen their use is interrupted reflex fluid retention occurs and thus, their use is perpetuated.49CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

– Persistent preoccupation with weight and figure: it is morbid dread of becoming fat. MostBN symptoms are secondary to these beliefs and their modification is probably essential toachieve complete resolution of the disorder 75 .4.2. Ethiopathogeny of eating disorders: what arethe main risk factors?Like other mental disorders, eating disorders have a multiple and somewhat uncertainethiology (yet unclear). According to studies, its ethiopathogeny involves several biologicalgeneticand vulnerability factors, psychological characteristics, sociocultural aspects andstressors. The specific impact of each one of them is yet to be determined.Eating disorders tend to begin in adolescence, although we are seeing a gradual increase inthe frequency of cases beginning in adulthood and childhood. These disorders usually affect thefemale population (for every 9 cases of eating disorders in women, there is 1 in men,approximately).At present, several risk factors have been determined for these disorders. The designs ofsome of the studies used have been cross-sectional and enable us to establish associations andnot causal relationships.Biological factorsResearch on biological factors has focused mainly on genetic factors and neurobiologicaldisturbances.Studies conducted on families show a higher frequency of eating disorders among relativesof individuals with eating disorders than among control subjects, leading to the conclusion thatthere must be family vulnerability to these disorders.Case-control studies using molecular genetics have found a positive association betweenthe presence of certain polymorphisms and a greater vulnerability to developing AN. The moststudied are the serotonergic system (5-HT; regulates appetite, stress response, sexual behaviour,obsessive symptomatology, mood, etc), the dopaminergic system and neurotrophins 76 (especiallyBDNF, NTRK2 77 and NTRK3 78 ).Equally positive results have also been obtained in chromosomes 1, 2 and 13. However,these results are not yet conclusive. Genes seems to account for 60% to 70% of vulnerability inthe case of AN 79 . In the case of BN, susceptibility is found in chromosome 10 80 . There isdiscrepancy regarding the early appearance of menarche as a risk factor in girls.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS50

Sociocultural factorsThe studies identified the following sociocultural factors as risk factors for eating disorders:overprotective, rigid and demanding, conflictive and poorly cohesive family models 81, 82 ,destructured families (divorced parents), family history of mood disorders and obsessivecompulsivesymptomatology 83 , eating disorders (especially in mothers), atypical dieting and/oreating behaviour in the family (parents concerned about weight) 84, 85 , obesity (especially inmothers) 85, 86 , alcoholism (especially in fathers), inconsistent eating habits during childhood 81 ,careers and/or activities during childhood-adolescence that place too much emphasis on slimnessand/or weight 87-89 .Psychological factorsThe following psychological factors have been associated with eating disorders: mooddisorders 90, 91 , personality disorders 92 , obsessive-compulsive disorders 93 , impulse controldisorder 94 , following an anomalous and restrictive diet and pre-occupation with the body,personal history of eating difficulties 85 , extreme rigidity, perfectionism, social alienation and lowself-esteem 95 .Potentially stressful life eventsRegarding the potentially stressful life events associated with eating disorders, thefollowing stand out: sexual and/or physical abuse during childhood, criticism towards one’sbody and a history of life crisis 85 .According to a review of eating disorder risk factors, some of the previously mentionedfactors have shown consistent results in the prediction of eating disorders, both in longitudinaland cross-sectional studies: gender, ethnicity (except Asians), eating problems andgastrointestinal disorders at early ages of childhood, sexual abuse and other adverse lifeexperiences, low self-esteem, general psychiatric morbidity, high weight and bodilydissatisfaction and dieting 97 .Of all the different explanatory models of AN, Garner’s (1993) 98 suggests that AN is theresult of the interaction of three types of factors: predisposing, precipitating and perpetuating.Predisposing factors confer susceptibility to AN.Some of these are determined by a genetic component, such as the female sex. Otherpredisposing factors are individual, family and cultural. Precipitating factors, such asdissatisfaction with body weight and shape, interact with predisposing factors in such a way thatthey condition affected individuals to the point where they decide they must lose weight andrestrict eating. Once AN has initiated, gradual weight loss leads to complications derived frommalnutrition. The disorder’s multidimensional consequences (physical, psychological and social)are both perpetuating factors of the disorder and boosters of predisposing and precipitatingfactors.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS51

Current literature suggests that eating disorders are partially determined by bothsociocultural 83, 84 and biological-genetic factors (the latter would explain 60%-70%) 99-101 . However,a part of the variance is not explained by any of these factors, leading to the performance ofstudies that assess the relevance of non-shared environmental factors which would explain whytwins, who have been raised in a similar family environment, can differ in terms of eatingbehaviour, pathological in some cases and normal in others. Amongst these factors, the followingwould be included: parents treating each sibling differently, the subjects’ personality andtemperament, the subjects’ relational style, experienced stressful situations and specificdifferential characteristics 81, 86 . Published scientific evidence shows that non-shared environmentalfactors are more relevant than shared factors. In this respect, 24% to 42% of variance in AN 102and 17% to 46% of variance in BN 90 would be explained by the influence of non-sharedenvironmental factors.4.3. What are the most frequent comorbidities in eatingdisorders?Comorbidity in eating disorders is common, both of mental and organic origin. The next sectiondescribes the most frequent associations. The therapeutic approach required in these cases willbe addressed in the chapter dealing with treatment.Substance-related disordersAbuse of illegal substances and chemical dependence is common in eating disorders, especiallyin BN and similar clinical pictures. In the beginning the use of stimulants (amphetamines andcocaine) is related with attempts to decrease appetite, but later it is linked with impulsivityassociatedBN pictures. Up to 40% of diagnosed patients (AN or BN) admit to abusing orhaving a dependence on alcohol or illegal substances 103-105 .Anxiety disordersAnxiety is so present in eating disorders it is hard to decide if it is a specific clinical componentof these disorders or if it is a comorbid condition. Eating disorders present specific phobiaclinical pictures (phobia of certain foods, social phobia, etc.) and others such as claustrophobiaor unrelated simple phobias. Panic attacks or anxiety crises present a similar situation. In somecases they are linked to eating disorders and in others they are truly comorbid. Studies reportvery varied anxiety prevalences that range between 10% and 40%, depending on themeasurement tools and inclusion criteria used 106-109 .Obsessive-compulsive disorder (OCD)Patients with eating disorders, especially AN, present significant prevalence of obsessivepersonality traits (See personality disorders). Many of these patients are rigid, strict, organized,responsible, constant, intransigent and intolerant, personality traits that predispose andCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS52

accompany eating disorders. However, in a considerable number of patients, up to 40% of themdiagnosed with AN, obsessive-compulsive disorder that meets comorbidity criteria is present 110-112.Personality disordersApproximately 30% of eating disorder cases present personality disorders 113-115 . There is a highprevalence of patients who meet BN criteria and present an associated personality disorder,especially borderline and histrionic.Mood disordersDepression is closely linked with eating disorders. It is hard to think of AN or BN without adepressive clinical picture. As in the case of anxiety, in some cases depression predisposes andin others it is linked with the clinical manifestation of eating disorders or presents itself as acomorbid condition. Prevalence of depression ranges between 40% and 80% and occurs morefrequently in BN 116, 117 .Impulse control disorderSome of the behavioural disturbances of eating disorders entail a loss of self-control (overeating,purging behaviour, self-aggression, etc.). Other impulse control disorders occur with eatingdisorders, such as kleptomania or trichotillomania 118, 119 .Diabetes mellitusDM is present in the genesis and evolution of eating disorders and also in treatment, whichwill have to be adjusted to this physical condition. Studies show very varied prevalence rates.Between 0.5% and 7% of cases of AN and BN present Type 2 DM. This percentage reaches upto 20% in EDNOS. Up to 9% of obese diabetics present an eating disorder 120-122 .Type 1 DM is a risk factor for eating disorders (three times more risk in BN and two timesmore risk in subclinical EDNOS 120 than the population without type 1 DM). Type 2 DM is a riskfactor for engaging in inadequate eating behaviours. When type 1 DM and an eating disordercoincide (OR: 4.8; 95% CI: 3.0 to 7.8) physical complication such as retinopathy increase. Inanother 4-year longitudinal study (N=91) on a cohort of patients with both pathologies (ED andtype 1 DM), 60% were associated with retinopathy 123 . In a further study conducted by Nielsen,2002 120 , mortality in patients with type DM at 10 years follow-up was 2.2 per 1,000inhabitants/year; in the AN population it was 7.3 and in the population with AN associated withtype 1 DM it was 34.4.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS53

ObesityObesity as a risk factor is linked to AN and BN. It is also a mid-long term habitual stateof BED and, in this case, obesity directly influences diagnosis and treatment. Up to 6% of obesechildren present BED 124-126 .Malabsorbtion syndromesEspecially in AN, malabsorbtion syndromes, gluten-intolerance or lactose-intolerance arerisk factors for eating disorders, course and prognosis modifiers and pathologies that must betaken into account when planning a treatment diet aimed at ponderal recovery. There are noprevalence studies and the literature only yields descriptions and studies of alienated cases 127, 128 .Thyroid diseasesThyroid diseases, both hyper and hypothyroidism, are relevant in the onset, course,prognosis and treatment of eating disorders. There are no prevalence studies, only casedescription studies 129-132 .CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS54

5. Prevention of Eating DisordersKey Questions:5.1. What is the efficacy of primary prevention interventions in avoiding eatingdisorders? Are there any negative effects?Primary prevention aims to limit the incidence of disease, in this case of eating disorders,by managing causes and exposure to risk factors or the patient’s increased resistance to these.Clearly, the first step to establish primary prevention measures is to identify relevant exposuresand assess their impact on the patient’s and the population’s risk of developing the disease.Specific primary prevention interventions for the most frequent eating disorders can beclassified in the following 5 types: psychoeducational, media literacy, dissonance-inductiontechniques, and interventions focused on eliminating eating disorder risk factors andstrengthening the host.In order to implement primary prevention measures there are two strategies, which oftencomplement each other: the population strategy and the high-risk strategy. The populationstrategy is general and is aimed at the entire population with the objective of reducing its averagerisk. The high-risk strategy is individual and is aimed at those people who most need it,meaning the most vulnerable individuals or those presenting additional risk as a consequence ofbeing exposed to certain risk factors. In the case of eating disorders, groups are considered ofrisk due to their age (adolescence), sex (female) or engagement in risk activities, be it as a hobbyor at a professional level (gymnasts, athletes, models, ballerinas, skaters, elite athletes, etc.) 133 .5.1. What is the efficacy of primary preventioninterventions in avoiding eating disorders? Are thereany negative effects?In order to respond to these questions, 4 high quality (1++) quantitative SRSE ormetaanalysis (MA) on eating disorder prevention programmes have been identified.Of the four MAs, one focuses the review on children and adolescents and only includesRCT 134 ; another one focuses on reviewing RCT and quasi-experimental studies (Q-RCT) onInternet-based prevention programmes 135 ; the others perform a general review of the topic,including RCT and quasi-experimental studies 136 . The potential iatrogenic effect (negativeimpact) of primary prevention programmes was another objective of two of these 4 MAs 134, 136 .The MA conducted by Stice E, et al. (2007) 137 includes all studies considered in the MAcarried out by Newton MS and Ciliska D published in 2006 135 ; 24/46 studies included in the MAconducted by Cororve FM, et al. (2006) 136 ; 10/12 studies included in the fourth MA conductedCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS55

y Pratt BM and Woolfendern SR (Cochrane Review), which was published earlier (2002) 134 .The search for RCTs has identified eight studies that were either published after or notincluded in previous MAs 138-145 . The eight RCTs assess high-risk strategies given that primaryprevention programmes are aimed at adolescents (men and women) 138 ; at adolescent women withbody dissatisfaction 141, 143, 145 , at female university students with subclinical levels of eating139, 140, 144pathology or who wish to improve their body image and female athletes 142 . The mostadministered intervention type was psychoeducational 138-140, 145 (in three of the studies the Internetwas used), followed by dissonance-induction techniques 143, 144 , critical assessment of mediacontent (media literacy) 141 and a specific programme called ATHENA (The Athletes TargetingHealthy Exercise and Nutrition Alternatives) 142 .The NICE CPG (2004) 30 did not address this aspect and only some protocols,recommendations and other documents on eating disorders elaborated by other organizations inour setting (See Annex 6.1.) tackled this aspect 10, 11, 13, 19, 146-151 , even though only the PAPPS 12 groupof experts formulates general recommendations.In the following section, the scientific evidence on primary prevention programmes foreating disorders is described.Scientific EvidenceIn a RCT (Stice, 2008; United States) conducted on a sample of 481 adolescentwomen (mean age: 17 years) with body dissatisfaction, the following interventionswere compared: dissonance-based thin-ideal internalisation reduction programme(group 1) vs. the healthy weight control programme (group 2) vs. expressive writingcontrol condition (group 3) vs. assessment-only control condition (group 4). Group 1showed significant reduction of thin-ideal internalisation, body dissatisfaction,negative affects and psychosocial impairment and lower risk for eating pathologyonset at 2- and 3- year follow-up vs. control subjects. In group 1 there was a greaterdecrease in thin-ideal internalisation, body dissatisfaction and psychosocial incapacitywhen compared to group 3. Group 2 showed greater reduction in all results, lessincreases in weight and lower risk of eating pathology onset at 2- or 3- year follow-upvs. control subjects. Group 2 showed greater decrease in weight and in thin-idealinternalisation than group 3.RCT1++At 3-year follow-up, participants in the dissonance programme showed a 60%reduction in risk for eating pathology onset; healthy weight participants showed a61% reduction; assessment-only controls showed a 55% reduction in risk of obesityonset. Therefore, the effect of such programmes is considered clinically importantand enduring in time.In a RCT (Jones M, 2008) 138 a population of adolescents (73 females and 22 males)from public schools in the US at risk for overweight was studied, and a specific 16-week Internet-facilitated intervention (StudentBodies2-BED)(N=52, 38m; 14v) wascompared to a wait list (N=53, 35m; 18v) with 9-month follow-up. The specificprogramme’s content combines psychoeducational and behavioural interventionsRCT1++56CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

(causal factors). Participants in the experimental group presented significant changesat baseline BMI (p

experimental group presented sustained effects in terms of their knowledge regardinga healthy diet and exercise, a reduction in their wish to be thin and decreaseddisordered eating at 3 months follow-up.The experimental programme was also effective in the group of women who were atrisk, resulting in favourable changes in the majority of variables. This studydemonstrates the benefits of using an Internet-based prevention programme andproves that transcultural adaptation can be successful.Based on the results of this MA, 51% of eating disorder prevention programmesreduce eating disorder risk and 29% reduce current or future eating pathology. Theseoverall percentages are favourable when compared to results obtained in other publichealth programmes (21% obesity prevention and 22% HIV prevention).The effect of prevention programmes was greater if the following characteristics weresatisfied: selected strategies aimed at high-risk populations (versus universal), aimedexclusively at women (versus both sexes), offered to participants over 15 years of age(versus younger people), interactive formats (versus didactic programmes), deliveredby trained professionals (versus endogenous providers, such as teachers or educators),with multiple sessions (versus single session), including contents on body acceptanceor the use of induction-dissonance techniques (versus psychoeducational orsociocultural interventions), assessed in trials using validated measures and, hence,more sensitive in determining the effect of interventions (only this type of measuresshould be used) and with shorter follow-up periods.In an RCT (Brien, 2006) 139 a population of 24 university females from Canada ofseveral different origins (58% Caucasian, 19% Hispanic and the rest of other origins),presenting subclinical levels of eating pathology, was studied. An 8-weekpsychoeducational intervention (N=13) was compared to self-monitoring control(N=11). Participants in the experimental group showed improvement in the scores ofdifferent specific questionnaires on eating disorders and other outcome measures thatwere significantly different from those observed in the control group.A psychoeducational intervention can alter the subclinical levels of eating pathologyin female university students from different cultures.In an RCT (Wilksch, 2006) 141 a population of young adolescent (mean age: 13.8 years)students in Australia (N=100 women and 137 males) was studied to compare onemedia literacy lesson vs. 6 lessons in the control group. Following the intervention,males had significantly lower values in 4/5 subscales of the questionnaire used tomeasure media internalisation, whereas females had significantly lower values in onesubscale. Higher baseline levels of dietary restraint, reading/buying magazines and aperception of sociocultural pressure predict lesser reductions in males’ scores,whereas depression predicts lesser reductions in females. Males must be included ineating disorder prevention programmes and media literacy is a promising approach toprimary prevention of eating disorders.In the only RCT (Elliot, 2006) 142 identified in a population of 1,179 female athletesstudying in schools in the US (mean age: 14.6 years), the ATHENA programme(N=457) was compared to a control group (standard treatments) (N=471). ATHENAMA ofRCTandQ-RCT1++RCA1+RCA1+RCA1++58CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

is a programme that promotes a healthy diet and physical exercise as alternatives toeliminate harmful practices. It consists of group sessions with educational material.Significant reductions were observed in the experimental group versus the controlgroup in terms of behaviours related with eating disorders and in the use of weightreduction drugs (p

(advocacy); and d) interventions related with self-esteem. 2 of the programmes basedon media literacy and mobilisation and social and political activism (advocacy)indicate a reduction in the internalisation or acceptance of societal ideals relating toappearance at 3- to 6-month follow-up (SMD:-0.28; 95% CI: -0.51 to -0.05). There issufficient evidence to support the effect of the 5 programmes that includeinterventions on eating attitudes and behaviours and other adolescent issues. There isalso sufficient evidence to support the effect of two of the programmes designed toimprove self-esteem.There is not enough evidence to indicate that harm resulted from any of theprogrammes included in this SRSE.Evidence SummaryMA 1371++This MA identifies the characteristics of eating disorder preventionprogrammes that produce the greatest effects.Programmes that are selected, interactive, multisession, offered solely towomen, offered to people over 15 years of age, delivered by trainedprofessionals, that incorporate contents related with body acceptance andinduction-dissonance techniques, that assess effects using validated measures,that do no include psychoeducational contents and have shorter follow-upperiods produce greater effects.MA 1371++MA 1371++MA 1351++MA 1361++MA 1361++MA 1361++There are several eating disorder prevention programmes that have also beenproven to be effective when delivered by teachers under valid ecologicalconditions.Some of the eating disorder prevention programs have had an effect on boththese disorders and obesity, which is promising from the point of view of publichealth.There is no consistent evidence regarding the impact of Internet-basedprevention strategies on eating disorder symptomatology and on the factors thatcontribute to the development of these disorders.Prevention programmes had a greater effect on improving knowledge and alesser effect on reducing incorrect behaviours and beliefs regarding eating.Studies aimed at high-risk populations produced greater benefits than thoseperformed on the general population (universal strategies).The results did not confirm the iatrogenic effects of includingpsychoeducational content on eating disorders in prevention programmes.60CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

MA 1341++MA 1341++No definitive conclusion was reached regarding the effectiveness of eatingdisorder prevention programmes, both aimed at the general population(universal strategies) and at high-risk populations (selective strategy), inchildren and adolescents.There is not sufficient evidence to suggest that any of the interventions includedin the MAs have a short-term negative impact (harmful effects).Recommendations 5.1. Sample, format and design characteristics of eating disorder programmes thathave demonstrated the highest efficacy should be considered the model forfuture programmes. 5.2. In the design of universal eating disorder prevention strategies it must be takeninto account that expected behaviour and attitude changes in children andadolescents without these types of problems may differ from those of higherrisk populations. 5.3. Messages on measures that indirectly protect individuals from eating disordersshould be passed on to the family and adolescent: following a healthy diet andeating at least one meal at home with the family, facilitating communicationand improving self-esteem, avoiding family conversations from compulsivelyturning to eating and image and avoiding jokes and disapproval regarding thebody, weight or eating manner of children and adolescents.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS61

6. Detection of Eating DisordersKey Question:6.1. What screening instruments are useful to identify eating disorder cases?6.1. What screening instruments are useful to identifyeating disorder cases?Eating disorders represent the third most common chronic disease in the adolescent patientpopulation. Additionally, the three types of eating disorders (AN, BN and EDNOS) are amongstthe three most common psychiatric diagnoses in adolescent females. Delayed identification ofeating disorder patients leads to higher morbidity due to delayed treatment, and hence, worseprognosis. It is important to identify people at high risk of developing an eating disorder inorder to tackle the disease at early stages and carry out an early intervention. To achieve thisgoal, involvement of primary care physicians is essential to detect symptoms and signs ofsuspected eating disorders.There are few studies on the detection and diagnosis of eating disorders in PC. Data pointto a situation of subdiagnosis, due to several reasons: scarce awareness of professionalsregarding this issue, the lack of real time resulting from health care pressure that impedesproviding better, more comprehensive care and preventive activities aimed at these patients, thelow attendance of adolescents to primary care practices and their lack of “disease awareness” 152 .Given these circumstances, the appropriate use of a brief and validated screeninginstruments during healthy children/adolescent consultations and those prior to performance ofsports would provide a good opportunity to apply prevention programmes for eating disorders,smoking, alcohol, drugs and safe sex in an integrated manner within a structured healthmaintenance programme from a family medicine approach.There has been some confusion regarding the use of screening instruments. They areinefficient to establish an eating disorder diagnosis, but are useful tools for a quick initialassessment aimed at ruling out suspicious symptoms in the first phase of the two stage screeningprocess, in which those patients who obtain high scores are newly assessed to determine if theyfulfil formal diagnostic criteria.To identify potential cases of eating disorders, several self-report screening questionnairesthat enable systematic assessment of eating behaviour have been designed. All of these includequestions regarding personal eating and dieting habits, weight, exercise, menstruation, bodyshape perception, self-image, self-esteem, drug use, relationship with the family and others,among other topics, given that most of the time patients with incipient eating disorders go to thedoctor due to other symptomatology, such as weight loss, amenorrhoea, depression, irritability,etc. Therefore, it is important to ask questions about these aspects.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS62

Of all the proposed criteria and recommendations for the assessment of the screeninginstruments, some authors determine their use/relevance, development and psychometricproperties and external validity to be the most important. Taking these considerations intoaccount, and based on the results of an SRSE published by Jacobi, et al. (2004) 153 , only a few ofthe self-report instruments labelled as screening instruments for eating disorders fulfil theaforementioned criteria.Of the screening instruments for identification of potential cases of eating disorders, fourfulfilled the criteria established by the previous SRSE: BET (Branched Eating Disorders Test)154, EDDS (Eating Disorder Diagnostic Scale) 155 , SED (Survey for Eating Disorders) 158 andSCOFF (Sick, Control, One, Fat, Food questionnaire) 157 . Only the latter has an adapted versionvalidated in our setting. At present there are no screening instruments that can differentiatebetween complete and partial eating disorders.Only one screening instrument for AN, the EAT-40 and its versions (EAT-26 and ChEAT),has high sensitivity and specificity, but its positive predictive value (PPV) is low for identifyingAN cases in the population. There are no questionnaires for screening of partial or subclinicalcases of AN.Of the three screening tools for BN: two-item screen 158 , only BULIT and BITE havesensitivity and specificity values for BN. However, the specificity of these questionnaires todifferentiate between BN and partial cases of BN and other eating disorders has not been clearlyascertained and population data are scarce.The following section describes the tools used for detecting eating disorder cases that meetall recommended criteria to achieve this goal:SCOFF SurveySick, Control, One, Fat, Food questionnaire.Morgan J, et al., 1999.The SCOFF is an eating disorder screening tool that consists of five yes/no questions that assessthe loss of control over eating, purging and body dissatisfaction (See Annex 2.1), thus enablingits application in primary care. Scores range from 0 to 5 points (No=0 and Yes=1). A totalscore of 2 or more points identifies people at risk of having an eating disorder (AN sensitivity:100%; BN: 100%; AN and BN specificity: 85% and 80%, respectively; false positive rate 7.3%for AN and 8% for BN) 157 . Independent studies performed in primary care indicate sensitivityvalues that range between 78% and 85% and specificity values that range between 88% and90%, with only affirmative answers 159, 160 . These are excellent results, especially because thequestionnaire is so brief. The reliability of the instrument when self-administered (written) orwhen administered by the physician (oral) was also assessed and results only evidenced minimaldifferences in SCOFF’s detection ability. However, the authors suggest that self-reportresponses may be more honest given that the patient’s confrontation with the interviewer isreduced 161 .CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS63

Spanish versionThere is an adapted Spanish version that has been validated in our setting by GarcíaCampayo J, et al., 2004 162 for early detection of eating disorders in primary care (women agedbetween 14 and 55 years with a cut-off point of 2 or more); sensitivity was 98% [95% CI: 93.5 to99.5] and specificity was 94% [95% CI: 86.4% to 98.5%]. For each specific eating disorder,sensitivities for 94% specificity were as follows: BN, 98%; AN, 93%; and EDNOS, 100%.Limitations relating to the adaptation of item 1 have been identified. It is recommended toreview these aspects before administering the Spanish version of SCOFF.A Catalan version has also been adapted and validated in our setting (SCOFF-c) by Muro-Sans P, et al., 2008 in a community sample comprised of Spanish adolescents (51% males and49% females; mean age=14 years; SD=1.31) 163 . In this study sensitivity was 73% (95% CI: 63.2to 82.9) and specificity was 94% (95% CI: 74.9 to 80.5). One of the possible reasons for lowsensitivity is sample characteristics (Barcelona youth who were recruited in PC).Of the numerous eating disorder screening questionnaires, results indicate the SCOFFsurvey can be a useful questionnaire given that it enables quick and easy primary care detectionof eating disorder risk groups in the community 164 . The SCOFF survey has been adopted as thestandard screening instrument in the UK 30 . Its characteristics also seem useful in monitoring thecourse of treatment (See Chapter 10, “Assessment”).EATEating Attitudes Test. DM Garner and PE Garfinkel, 1979.The EAT was designed for the assessment of disordered eating attitudes, especially those relatedwith fear of gaining weight, the impulse to lose weight and the presence of restrictive eatingpatterns. Its intention was to devise an instrument that was easy to use and easy to correct andthat was sensitive to symptomatic changes throughout time. The EAT is a self-report toolcomprised of 40 items (EAT-40). Each item is valued in a 6-point Likert scale that ranges from“never” to “always”. Scores range from 0 to 120. It is a valid and reliable questionnaire that hasbeen widely used in the assessment of eating disorders. With the 30 point or more cut-off pointin a group of AN patients and a control group, sensitivity was 100% and specificity was 84.7%,with a PPV of 78.5% and a false-positive rate of 9.8% 165 .Other studies had revealed that the EAT test can be useful for the detection of AN casesthat have not been previously diagnosed or to identify current or incipient cases of AN in highrisk populations (ballerinas, model trainees, for example) with sensitivities, specificities andPPVs that range between 75% and 91.7%, 66.1% to 75% and 16% to 18.8%, respectively, withfalse-positive rates between 23.2% and 31.7% 97 . Of all the different instruments that have beendeveloped since the 70s up until today, the EAT-40 has been the most widely endorsed for thedetection of eating disorders in the general population, and it is an instrument that seems valid toidentify current or incipient cases of AN and BN, given its easy application, high reliability,sensitivity and transcultural validity.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS64

Spanish version of the EAT-40In Spain, the adapted version of the EAT-40 that was validated in our setting was carriedout by Castro J, et al. 1991 in an AN group and healthy control group 166 (See Annex 2.2). Usingthe 30-point cut-off point recommended by the original authors, sensitivity was 68% andspecificity was 86%. Among the possible causes that may explain differences with the originalversion, the fact that Spanish anorexic patients were younger must be highlighted. When it wasvalidated in a sample of 18-year old women using the questionnaire by Castro J, et al. and the30-point cut-off point, sensitivity was 75%, specificity was 97.1% and PPV was 36% 167 .In Navarra, another study to validate the adaptation by Castro J, et al. after an 18-monthfollow-up was performed on a representative sample of adolescent students who did not attendthe doctor’s office but came from the general population instead, once prevalent cases of eatingdisorders were excluded 168 . With a cut-off point of 20 points, better diagnostic prediction wasobtained (73% sensitivity and 85% specificity). PPV was 20% and the negative predictive value(NPV) was 98%.From these results we can conclude that the EAT-40 is an adequate questionnaire for earlydetection of eating disorders in the general population, even if its PPV is low. However, despiteusing screening instruments it is always necessary to conduct individual interviews to confirmdiagnoses of eating disorders. The fact that eating disorders are presented in a grading andseverity continuum makes it essential to have a procedure that enables the detection of earlysigns to ensure a prompt intervention.EAT-26 (Abbreviated version of the EAT-40)Garner DM, et al., 1982 created the 26-item version of the EAT-40 by performing a factoranalysis of the latter. The EAT-26 is highly predictive of the complete version (r=0.89). Itconsists of the first 26 items of the EAT-40, configuring three subscales: diet, bulimia andconcern over eating and oral control. It is assessed using the same 6-poing Likert scale as theEAT-40. Answer scores range from 0 to 78. It is a self-report questionnaire 169 . Using a cut-offpoint of 22 points or more, the range of sensitivities, specificities and PPVs was 65.1% to 88.9%,96.1% to 97.7% and 44.4% to 46.2%, respectively, the false-positive rates ranging from 2.7% to3.8% 97 .Spanish version of the EAT-26The Spanish validation of the EAT-26 in our setting was carried out by Gandarillas A, etal., 2003 in a community setting on a female student population (15-18 years) (See Annex 2.3.).The psychometric characteristics of this questionnaire are similar to those described by theirauthors. For a 20-point or more cut-off point, sensitivity is 59%, specificity is 93%, PPV is23%, NPV is 99% and the percentage of correctly classified subjected is 92% 170, 171 . As ascreening questionnaire it is useful to differentiate eating disorder cases from the normalpopulation, although it is important to mention the scarce PPV, given the low prevalence of theproblem 170, 171 .When the cut-off point is lower (10 points or more), the EAT-26 presents 90% sensitivity,CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS65

75% specificity, 11% PPV, 99.5% NPV and a percentage of correctly classified subjects of76% 170, 171 .The MSC already recommended its use as a screening tool back in 1995 20 because the EAT-26 was able to distinguish between AN patients and normal population and between BN patientsand normal population, but not between restrictive AN and BN, establishing a cut-off point of30 in high risk population and >50 in clinical population 20 .ChEAT (Child version of the EAT-26; Children Eating Attitudes Test)Maloney MJ, et al., developed the ChEAT 1988, with the aim of detecting comprehensionproblems in children. When these problems were resolved by substituting certain words withsimpler synonyms, validity and reliability results in a sample of children between the ages of 8and 13 years were comparable to those published for adults (EAT-26), making the ChEAT aself-report questionnaire that can be administered starting at 8 years of age (it does require a 5thgrade reading level in order to answer), which can aid in the assessment of concern over food,eating models and attitudes regarding food at these ages. A total score of 20 points in the upperscale would indicate the possible presence of an eating disorder 172 .Spanish version of the ChEAT (Children’s Eating Attitudes Test)The Spanish adaptation and preliminary validation of the ChEAT has been carried out byde Gracia M, et al., 2008 on a sample of girls and boys between the ages of 8 and 12 years.Reliability and validity results of the Spanish adaptation are analogous to the original study 173(See Annex 2.4.).The Catalan version of the ChEAT has also been adapted and validated in our setting in asample of students (5th and 6th grades). Results indicate that the Catalan version is reliable.However, it is recommended that the cut-off point be lower than that established by the originalauthors, as was already suggested by the authors of the Spanish adaptation, given that itincreases the number of subjects at risk of developing an eating disorder that may be detected atschool 174 .BULIT Bulimia TestBulimia Test. MC Smith and MH Thelen, 1984.The BULIT was designed with the objective of addressing certain needs detected in theassessment of BN, such as distinguishing BN patients from people without eating disorderproblems; BN patients from patients with other eating disorders, and BN sub-groups based onspecific criteria. It consists of 32 items (plus four informative type items relating to laxativeabuse, use of diuretics, as well as amenorrhoea) that are distributed in five dimensions (bingeeatingepisodes or lack of control over meals, discomfort, vomiting, type of food and weightfluctuation). Each item is scored using a 5-point Likert scale (ranging from 1 to 5). In severalitems the most symptomatic answer is presented at the end rather than at the beginning toprevent a bias in the response, due to presentation order. The sum of all items (except the purelyinformative ones) leads to an overall score ranging from 32 to 160 (a higher score indicatesgreater intensity of bulimic symptomatology). Likewise, the sum of items corresponding to each66CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

of the five dimension results in the overall scores for each one of these dimensions. An overallscore and five scores corresponding to each dimension are therefore obtained. Data derivedfrom the original version indicates that it is a reliable, valid and objective instrument to identifyindividuals with bulimic symptoms, confirming its use to detect those individuals who present orwho are at risk of developing BN in the general population 175 . With a cut-off point of 102 pointsor more, sensitivity, specificity, PPV and NPV were 95%, 98%, 91% and 99%, respectively.Spanish version of the BULITIn Spain, the adapted version of the BULIT validated in our setting was developed by AJVázquez, et al., 2007 in a group of people, mainly females between the ages of 13 and 54 years,who attended mental health centres 176 (See Annex 2.5.). Results solidly support the reliabilityand validity of the Spanish version of the BULIT, highlighting its use to identify BN cases, aswell as to quantify the severity of bulimic symptoms. With a cut-off point of 88, it leads to a90% correct classification of individuals with BN, and a 100% correct classification ofindividuals without eating disorders, data that firmly endorse its use as a screening instrument.BULIT-R (Revised version of the BULIT)Later, the revised version of the BULIT (BULIT-R), developed by Thelen, et al., 1991 wasobtained, its most important contribution being the adaptation to DSM-III-R and later DSM-IVcriteria 177 . It is comprised of 36 items, even though only 28 are used to determine the final scorethat ranges between 28 and 140 points. The estimated administration time of the instrument is10 minutes. It is highly correlated with the original version (r=0.99). In a sample of nursingstudents and with a cut-off point of 104 points or more, sensitivity, specificity, PPV and NPV ofthe BULIT-R was high: 80%, 99.5%, 80% and 99.5%, respectively 178 .Spanish version of the BULIT-RIn Spain, the adapted version of BULIT-R validated in our setting was carried out by MNBerrios-Hernández, et al., 2007 179 .BITE Bulimia Investigatory Test Edinburgh. M Henderson andCPL Freeman, 1987.The BITE is a self-report questionnaire completed in 10 minutes or less that is designedto identify subjects with bulimic symptoms (BN or BED). It consists of 36 items that configuretwo subscales: the symptoms scale (assesses the number and degree of existing symptoms; 30items; highest score: 30; cut-off point: 20 points or more) and the severity scale (provides adisorder severity index based on the frequency with which pathological behaviours take place; 6items; highest score: 39; cut-off point: 5 points or more). A total score of 25 or more pointsindicates the presence of a serious eating disorder. In the sample of bulimic women and controlgroup the cut-off points used were as follows: >25 for the complete questionnaire, >20 for thesymptoms subscale and/or >5 points for the severity scale. With these cut-off points, the BITEdemonstrated perfect sensitivity, specificity and PPV (100%, 100% and 100%, respectively),even though data on its use in the population are not known 180 .67CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Spanish version of the BITEThe adapted version validated in our setting was developed by T Rivas, et al., 2004 181(See Annex 2.6.).The Spanish version of BITE was administered to a sample of adolescents aged between12 and 21 years from different schools. Using cut-off points based on DSM-IV criteria for BN,high specificity and a much lower sensitivity than that found in clinical samples were obtained.Furthermore, the scores in the BN group were higher than in other eating disorders and in thegroup without eating disorders. Therefore, this instrument can be used for early detection ofindividuals who may present an eating disorder in the general population. It is also used toassess disease intensity and response to treatment.RecommendationsD 6.1. Target groups for screening should include young people with low body massindex (BMI) compared to age-based reference values, patients consulting withweight concerns without being overweight or people who are overweight,women with menstrual disorders or amenorrhoea, patients with gastrointestinalsymptoms, patients with signs of starvation or repeated vomiting, and childrenwith delayed or stunted growth, children, adolescents and young adults whoperform sports that entail a risk of developing an eating disorder (athletics,dance, synchronised swimming, etc.). (Adapted from recommendation 5.2.5.3of the NICE CPG).D 6.2. In AN, weight and BMI are not considered the only indicators of physical risk.(Adapted from recommendation 5.2.5.6 of the NICE CPG).D 6.3. Early identification and intervention of individuals presenting weight loss areimportant to prevent the development of severe emaciation. (Adapted fromrecommendation 6.6.1.2 of the NICE CPG).D 6.4. In the case of suspected AN, attention should be paid to overall clinicalassessment (repeated over time), including rate of weight loss, growth curve inchildren, objective physical signs and appropriate laboratory tests. (Adoptedfrom recommendation 5.2.5.7 of the NICE CPG).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS68

6.5. It is recommended to use questionnaires adapted and validated in the Spanishpopulation for the detection of eating disorder cases (screening).The use of the following tools is recommended:Eating disorders in general: SCOFF (for individuals aged 11 years and over)AN: EAT-40, EAT-26 and ChEAT (the latter for individuals aged between 8 and12 years)Bulimia nervosa (BN): BULIT, BULIT-R and BITE (all for individuals aged12-13 years and over) 6.6. Adequate training of PC physicians is considered essential for early detectionand diagnosis of eating disorders to ensure prompt treatment, or referral, whendeemed necessary. 6.7. Due to the low frequency of consultations during childhood and adolescence, itis recommended to take advantage of any opportunity to provide comprehensivecare and to detect eating disorder risk habits and cases. Eating disorder riskbehaviour, such as repeated vomiting, can be detected at dental check-ups. 6.8. When interviewing a patient with a suspected eating disorder, especially if thesuspected disorder is AN, it is important to take into account the patient’s lackof awareness of the disease, the tendency to deny the disorder and the scarcemotivation to change, this being more pronounced in earlier stages of thedisease. 6.9. It is recommended that different groups of professionals (teachers, schoolpsychologists, chemists, nutritionists and dieticians, social workers, etc.) whomay be in contact with at-risk population have adequate training and be able toact as eating disorder detection agents.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS69

7. Diagnosis of Eating DisordersKey Questions:7.1. What clinical criteria are useful to diagnose eating disorders?7.2. How are eating disorders diagnosed?7.3. What is the differential diagnosis of eating disorders?7.1. What clinical criteria are useful to diagnose eatingdisorders?Clinical criteria for the diagnosis of AN and BN are well defined in the InternationalStatistical Classification of Diseases and related health problems, tenth edition (ICD-10) of theWorld Health Organisation (WHO, 1992) 182 and in the Diagnostic and Statistical Manual ofMental Disorders, fourth edition (DSM-IV) and text revision (DSM-IV-TR) of the AmericanPsychiatric Association (APA, 1994 183 and APA, 2000 184 , respectively).The DSM-IV/DSM-IV-TR classifies mixed and partial forms of eating disorders, such asEDNOS, where BED is included, while the ICD-10 refers to them as atypical AN, atypical BNor unspecified eating disorders.The DSM-IV/DSM-IV/TR, in contrast to the ICD-10, differentiates between two types ofAN (restricting and compulsive/purging) and two types of BN (purging and non-purging)depending on the predominant behaviour.The Spanish versions of these classification systems have been subsequently edited: ICD-10 (2000) 185 and DSM-IV-TR (2008) 186 . In the latter, the equivalent between classifications ispresented (DSM-IV-TR, ICD-9 and ICD-10). In Annex 2.7. diagnostic criteria according to bothclassifications are described.Recommendation 7.1. It is recommended to follow the diagnostic criteria of the WHO (ICD-10) andthe APA (DSM-IV or DSM-IV-TR).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS70

7.2. How are eating disorders classified?The diagnosis of eating disorders is based on a clinical interview complemented bycomplementary physical, psychopathological and behavioural examinations aimed at assessingthe existence of physical, emotional, behavioural and cognitive disturbances. Diagnosis hasgood validity and reliability.AnamnesisWhen an eating disorder is suspected, both a personal and family complete clinical historymust be performed. Given that patients are usually young adults and adolescents, theseinterviews must have certain specific characteristics to overcome the difficulties derived from aperson’s willingness to reveal his/her motives, symptoms and behaviour, sometimes an obstacleto making a diagnosis. Thus, the empathy, support and compromise that is perceived during theclinical interview will be essential in enabling the patient to reveal fears regarding weight gain,eating behaviour, purging behaviour and other disordered behaviour such as excessive exercise.When deemed appropriate, this clinical history must be accompanied by a corroborative accountfrom parents or other relative.After explaining the reason for the consultation, if patients are accompanied by theirfamily, the latter must be asked to leave the room to generate a climate of privacy where thepatient can freely respond to the questions asked (See chapter 12, “Legal Aspects”).The confidentiality of the medical act must always be emphasised, making it clear to thepatient that none of what is discussed between him/her and the health care professional will bedisclosed to parents or family members unless otherwise specified by the patient, except whenthere is risk to the patient’s physical or psychological integrity (See chapter 12, “LegalAspects”). The performance of blood work and other tests must be agreed upon with the patient.The health care professional will try to be perceived as somebody who looks after the patient’shealth, and not as an ally to the family. The patient’s genogram and whom he/she lives withmust be known. To this end, family and personal pathological history must be requested(especially if it relates to mental health: depressions, phobias, addictions, eating disorders,physical and psychological abuse).During the anamnesis, questions will be asked regarding physical disorders (weight, skinand mucosa, menstruation), emotional disorders (anxiety, depression, social alienation, eatingdisorder triggers [see chapter 4, “Definition and Classification of Eating Disorders], sleepdisorders), behavioural disorders (diets, exercise, binge-eating, extravagance with food, personaland family eating habits, purging behaviour, physical hyperactivity) and cognitive disorders(image distortion, disease awareness).The semi-structured interviews most frequently used to diagnose eating disorders are 187 :section H (for eating disorders) of the diagnostic interview Composite International DiagnosticInterview (CID-I) developed by the WHO, 1990 188 and Eating Disorders Examinations (EDE)developed by Cooper and Fairburn, 1987 189 .CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS71

Although these two interviews are adapted to diagnostic criteria defined by the DSM-IV-TR and the ICD-10, there is consensus that the most reliable and best validated semistructuredinterview for the diagnosis of eating disorders is the EDE. The 12th edition of the EDE (EDE-12) developed by Fairburn and Cooper, 1993 19O has a Spanish version, adapted by MR Raich,1994 191 and validated in our setting 192, 193 on a sample of 99 female university students, that hasproven to be a reliable and valid tool. Another adaptation and validation of the EDE on a samplein our setting, performed by Robles, et al., 2006 194 , has been identified, presenting appropriatepsychometric qualities that are similar to those of the original version (See Annex 2.8., EDE-12).There are preliminary results of the child version of the EDE-12 (ChEDE-12) on a sampleof 15 children with AN and 15 with other eating disorders and two age-adjusted groups of 15control subjects. Preliminary results indicate that the ChEDE-12 differentiates children with ANfrom children with other eating disorders and from control subjects 195 . There is no informationregarding the adapted version validated in our setting in these ages.During the anamnesis it may also be helpful to ask only the items relating to the diagnosticcriteria of eating disorders described in the ICD-10 and DSM-IV-TR. This measure, which hasbeen employed frequently in the literature, facilitates the diagnostic process, as well as thepatient’s participation, without compromising diagnostic efficacy. With this restriction, theduration of interviews is reduced to ten or fifteen minutes per person.Informing the patient with an eating disorderAs usual, when informing the patient on his/her disease, care must be taken in how themessage is conveyed, adjusting it to the patient’s age, educational level and beliefs, amongstother aspects. To make this task easier for the health care professional, this CPG providesmaterial aimed at children, adolescents and adults with eating disorders or who are at risk ofdeveloping them. This material may also be useful to family members, friends or people whointeract with patients, as well as for the general population (See Annex 3.1.).The diagnosis of an eating disorder must be communicated clearly, describing theimportant characteristics of this mental disorder. It is also helpful to explain the physicaldimensions and disturbances it causes, as well as its evolution and prognosis.The patient must not be made to feel guilty. However, it must be clearly explained thathe/she is suffering from a disease, that it is treatable and curable but that his/her involvement iscrucial for recovery.Anamnesis and family awarenessIt is very important to study the family environment and detect possible disturbances in itscorrect functioning (disorganised families, strict rules, etc.). Other family-related risk factorsmust also be assessed (mothers who are very critical of physical appearance, family conflicts, ahistory of weight loss diets in other family members, especially the mother, etc.) (See chapter 4,“Definition and Classification of Eating Disorders” and chapter 11, “Prognosis”).Communication with the family must be established to explain eating disorders, toemphasise that their active involvement in the patient’s treatment and recovery process is crucial,CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS72

to help them cope with the situation and to make them aware that positive changes in the familyroutine must be made (for example, strengthen the patient’s maturation, autonomy andresponsibility processes, by establishing rules and guidelines adjusted to the child’s age, stimulatethe expression of both positive and negative feelings). The patient information elaborated for thisCPG can be useful (See Annex 3.1.).Eating Disorders in AdultsWhen faced with potential cases of eating disorders in adults, clinical history questionsshould be adapted to a conventional interview with an adult, who is responsible for his/her actsand decisions, who meets with the health care professional alone most of the time, and wherehe/she usually prefers the family not to be involved.The adult patient’s economic independence enables easier access to harmful or toxic drugs,which is why the patient’s personal toxicopharmacological background must be emphasised inorder to detect abuse or misuse of substances.In these cases, it is also more likely to find work-related, economic or social problems asmaintaining factors or, sometimes, as eating disorder triggers.It is important to highlight that there are also thin, non-pathological constitutions that arewell-adjusted to development.Physical explorationPhysical exploration is less useful than anamnesis in establishing diagnosis. However,complete physical exploration is crucial and must be aimed at assessing the patient’s nutritionalstate and detecting possible secondary physical complications resulting from dietary restraintsand/or purging behaviour that would determine the intervention of other specialists or not.Data corresponding to vital signs (heart rate, blood pressure, axillary temperature andrespiratory rhythm) will be collected; in patients with a certain degree of malnutrition these signswill be in the lower limits. For weight and size, the BMI (BMI=weight kg/size m 2 ) will bedetermined. If the BMI is >25 it is considered overweight; if it is between 25-18.5 is considerednormal, and if it is

dental erosion, enamel demineralisation and cavities.- Cardiocirculatory examination. An electrocardiogram must be performed on patients with ANand signs of malnutrition and also on patients with BN at risk of dyselectrolytemia. Bradycardiamay be found. Hypopotasemia may cause a U-wave, T-wave flattening/inversion, prematureventricular contractions and ventricular arrhythmias, and hypomagnesemia can also producearrhythmias.- Respiratory examination. Possible opportunist infections. In patients who vomit, possiblepneumothorax or even aspiration pneumonia.- Neurological exploration. Detection of possible polyneuropathies secondary to vitamindeficiency, detection of neurological symptoms secondary to hypopotasemia and detection ofaqueous intoxicationPsychopathological and behavioural examinationIn the psychopathological and behavioural examination different instrument can beadministered with the objective of assessing eating behaviour and the psychopathologicalsituation (impulsivity, anxiety, depression, personality and obsessiveness). (See chapter 10,“Assessment”).Complementary examinationsBased on the results of the physical exploration, further examinations that includelaboratory tests and other explorations can be performed. However, an excess of examinationsto confirm treatment may be counterproductive.Laboratory testsBlood work should include the following parameters: hemogram, glycaemia, totalcholesterol, triglycerides, liver enzymes (AST, ALT and GGT), ions (K, Na, Cl, Ca, P and Mg),total proteins and albumin, creatinine and urea, TSH, free T3 and T4, coagulation (TP, TTPa),urine (sediment and osmolarity) and female hormone profile.The analytical examination of eating disorders enables the ruling out of possible organiccauses of weight loss and for the patient to pick up his/her results, making a new kind of weightmanagement and more time for a detailed interview on losing weight possible.A normal analysis can never rule out an eating disorder. In these cases, it can becounterproductive given that it can favour “false tranquillity” in the patient, family and nonspecialisedexpert; it can become a positive reinforcement for the patient’s attitude; or, thepatient may even view the professional as an ally of the family.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS74

Other examinationsTo ascertain whether there are bronchoaspirative lesions in patients who vomit a chest x-ray will be requested, as well as when other pathologies such as tuberculosis are suspected.Bone x-ray and densitometry enable the assessment of bone age in people in development andthe presence of osteoporosis or osteopenia. Electrocardiography, amongst other tests, isindicated when there is suspicion of laxative abuse. The decision to perform more sophisticatedexaminations is left to consulting specialists.Diagnostic difficulty is greater in cases where there are comorbidities. The most frequentcomorbidities are: diabetes mellitus, obesity, malabsorbtion syndrome and thyroid diseases oforganic origin and substance abuse and dependence, mood disorders, obsessive-compulsivedisorders, personality disorders, as well as impulse control disorders.RecommendationsD 7.2.1. Health care professionals should acknowledge that may eating disorder patientsare ambivalent regarding treatment due to the demands and challenges that itentails. (Adapted from recommendation 1.10.1.1 of the NICE CPG).D 7.2.2. Patients and, when deemed necessary, carers should be provided withinformation and education regarding the nature, course and treatment of eatingdisorders. (Adapted from recommendation 2.10.1.2 of the NICE CPG).D 7.2.3. Families and carers may be informed of existing eating disorder associationsand support groups. (Adapted from recommendation 2.11.5.5 of the NICECPG). 7.2.4. 7.2.5.It is recommended that the diagnosis of eating disorders include anamnesis,physical and psychopathological examinations and complementaryexplorations.Diagnostic confirmation and therapeutic implications should be in the hands ofpsychiatrists and clinical psychologists.75CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

7.3. Differential Diagnosis of Eating disordersDespite the existence of certain well-defined diagnostic criteria for eating disorders, inclinical practice there are often difficulties relating to the differential diagnosis with otherconditions that require rigorous clinical assessment.In regards with AN, the differential diagnosis must be made with those pathologies that canpresent significant appetite loss and weight loss, even though the main features of AN, such asbody image distortion, the desire to perpetuate weight loss and the fear of becoming fat, are notpresent in all cases:• Mental disorders: depression, anxiety, psychotic disorders and substance abuse• Diabetes mellitus• Tuberculosis• Hyperthyroidism• Neoplasias of the central nervous system• Less frequent: lymphomas, sarcoidosis, Addison’s disease, celiac disease, superiormesenteric artery syndrome (it may sometimes be a complication of AN), AIDS, lactoseintolerance, panhypopituitarism, etc.The differential diagnosis of AN is especially indicated in adult patients, given the atypicalage of onset of the disorder.The differential diagnosis of BN is more limited than AN and includes organic conditionsthat present hyperphagia and weight gain:• Diabetes mellitus• Hypothyroidism• Kleine-Levin Syndrome (idiopathic disorder that especially affects men aged 20-30 yearsand that presents with hypersomnia and hyperphagia).• Hypothalamic lesions• Tumours causing hyperphagia• Major depression, atypical depression, borderline personality disorder (BPD).The differential diagnosis of EDNOS must be performed with pathologies that may presentwith weight loss or gain and/or decreased or increased appetite. The differential trait of EDNOSis body-scheme distortion and excessive and irrational focus on weight and diet.In BED, the differential diagnosis must be performed with the same pathologies describedfor BN and with clinical pictures of impulse control disturbance that may present with bingeeatingepisodes, such as those that occur in BPD.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS76

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8. Interventions at the Different Levels ofCare in the Management of EatingDisordersKey Questions:8.1. What are the primary care (PC) and specialised care interventions for eatingdisorders? Other resources?8.2. In eating disorders, what clinical criteria may be useful to assess referralamongst the health care resources available in the NHS?8.3. In eating disorders, what clinical criteria may be useful to assess completehospitalisation (inpatient care) in healthcare resources available in theNHS?8.4. In eating disorders, what clinical criteria may be useful to assess discharge inhealth care resources available in the NHS?8.1. What are the primary care (PC) andspecialised care interventions for eatingdisorders? Other resources?The management model proposed, in which patients are referred from one managementresource to another, is bound by protocols, recommendations and guidelines elaborated withclinical criteria for which there is little evidence that guides decisions regarding where toperform the intervention (See question 8.2. in this chapter).8.1.1. Primary Care (PC) interventionsPrimary care is carried out in primary care centres, the first level of access to health care. At thislevel interventions are focused on:– Identifying individuals at risk of developing an eating disorder (See chapter 6, “Detection”)and establishing an early diagnosis (See chapter 7, “Diagnosis”).– Deciding whether the disorder can be treated in the primary care centre or whether it must bereferred to specialised care. In order to make this decision, the patient’s type of eatingdisorder, age, level of risk, physical and psychological complications and preferences must betaken into account.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS78

– Initiating nutritional treatment that includes the following objectives: restoring normal weightin the patient, correcting malnutrition, avoiding the refeeding syndrome, managing or curingmedical complications, carrying out nutritional education with the objective of normalisingaltered dietary behaviour, both in the patient and in his/her family, and preventing andmanaging recurrences.Initiating nutritional restoration by means of adequate renutrition or refeeding (See question 9.1.chapter 9, “Treatment”) and performing nutritional education (nutritional counselling) (Seequestion 9.2. chapter 9, “Treatment”).– Monitoring cases that are managed in primary care centres (in AN: the patient will berequested to record daily consumption, hyperactivity, laxative abuse and use of diuretics;he/she will be not be allowed to weigh him or herself and weight will be recorded weekly atthe practice, results to which the patient will not have access; in BN: binge-eating episodes andself-induced vomiting, substance abuse and other behaviour disorders (impulse, etc.) will berecorded, as well as recurrence prevention.– Conveying clear and true information regarding eating disorders to patients and relatives (SeeAnnex 3.1.). Also detecting and correcting maladaptive ideas about weight and health (SeeAnnex 2.9.).– Carrying out interventions with affected families (See chapter 7, “Diagnosis”).– Managing physical complications (See chapter 9, “Treatment”).8.1.2. Specialised care interventionsEating disorder patients are provided with specialised care, the second and third levels of accessto health care, in the form of inpatient care resources (psychiatric and general hospital),specialised outpatient practices (mental health centres for adults and children), day hospitals forday care (centres specialised in eating disorders and general mental health centres), emergencyservices, medical services pertaining to general hospitals and specific units (for eating disorders,borderline personality disorder and toxicology).– Assessment and diagnosis visits are performed at an outpatient level (CSMA and CSMIJ) afterreferral from PC. In the case of vital emergencies or autolytic risk that stand in the way of thisassessment, the patient must be referred to internal medicine and psychiatry services and willbe admitted if indicated by the physicians on-duty.– The clinical history must update and complete what has been established in PC.– After establishing a diagnosis, the mental health team will design an ITP which includes: a)definition of the problem based on the diagnosis and altered areas, b) formulation ofpsychotherapeutic objectives, c) election of treatment (psychological therapies,pharmacological treatments, medical measures and social interventions) (See the “treatment”CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS79

section), and d) time-frame for therapeutic assessment. Following the therapeutic decision, theITP will be presented to the patient and family, informing them on: a) health care professionalswho will be involved in treatment, b) techniques that will be employed, c) duration, and d)time-frame for assessment.The degree of nutritional deterioration, along with the presence or absence ofcomplications, determine the selection of access and feeding route, as well as the location wherenutritional follow-up must be performed.The day care treatment programme includes meal monitoring, and patients must complete asurvey on the foods they ingest in 24 hours, including on weekends when they are away from thecentre. Each patient must be medically and nutritionally assessed at least once a week, weightand related medical symptoms must be monitored, requested blood work must be assessed ifnecessary, and the dietary survey and objectives must be reviewed. In inpatient care, nutritionalsupport with artificial nutrition must be strictly monitored to avoid or manage the onset of therefeeding syndrome.8.1.3. Other resourcesMutual help groups (MHG) are groups of people who meet voluntarily with the aim ofhelping each other. They are generally comprised of individuals who share the same problem orwho find themselves in a similar difficult situation. The MHG emphasises personal interactionand each member’s capacity to assume responsibilities. It tends to provide emotional help andpromote values that help members strengthen their own sense of self. These groups provideassistance and emotional support to families and patients, facilitating the success of thecorresponding therapy. Groups are guided by facilitators (people who have experienced thesame problem or situation as the participants) and are periodically aided by a professional whosupervises the intervention and provides instruments to improve group dynamics (See Annex3.2. Support associations for patients with eating disorders and their families).Counselling consists of performing a series of personal interviews with patients andrelatives to inform and educate on the disease and its main health, family and socialconsequences, as well as to provide guidance on the current situation of health care, legal,economic and social resources, with the objective of reassuring and assisting the patient and/orfamily.Day centres are public sociosanitary resources that accommodate patients with differentlong-term disorders, including cases of chronic eating disorders and cases with psychiatriccomorbidity. These centres provide, amongst other activities and interventions, rehabilitation(tertiary prevention). In our setting there are no public day centres aimed exclusively at patientswith eating disorders.Therapeutic apartments (assisted or not) constitute another public network resource thatenables social reinsertion of patients suffering from different disorders. In our public networkthere are no apartments specifically for eating disorder patients.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS80

8.2. In eating disorders, what clinical criteria may be usefulto assess referral amongst the health care resources availablein the NHS?8.2.1. Referral to mental health servicesCriteria for referral from primary care to mental health services (CSMA and CSMIJ) are asfollows:• When there is an established diagnosis of eating disorder.• Weight loss equal to or higher than 10%-25% of weight, without a cause to account for it.• Presence of regular bulimic episodes, meaning over-eating and/or persistent purgingbehaviour (self-induced vomiting, laxative abuse and use of diuretics).• Presence of associated psychopathological disturbances.• Lack of disease awareness.• If, despite following PC indications, weight and bulimic behaviour do not improve.8.2.2. Referral to emergency hospitalisationCriteria for referral from primary care to emergency hospitalisation (Emergency service of ageneral hospital) to receive emergency medical treatment are as follows:• Weight loss >50% in the last 6 months (30% in the last 3 months).• Consciousness disturbances.• Convulsions.• Dehydration.• Severe liver or kidney disturbances.• Pancreatitis.• Decreased potassium

8.3. In eating disorders, what clinical criteria may beuseful to assess inpatient care (completehospitalisation) in one of the health care resourcesavailable in the NHS?8.3.1. Inpatient care (complete hospitalisation) criteria• Biological state that entails a risk of serious complications (no food intake, especiallyliquids, BMI

8.3.2. Criteria for admission to day patient care (day hospital)• From the adult or children MHC. If the patient does not meet emergency medical care oremergency psychiatric admission criteria and does meet any of the following criteria:– The patient is unable due to the psychopathology presented to follow the guidelines inthe outpatient programme: frequency of visits, limitation of physical activity,recommended diet, etc.– There are serious behavioural problems at home, conflicts in family relationshipsand/or family psychopathology that cannot be modified at an outpatient level.– Weight evolution does not follow the rate indicated in the outpatient programme forweight restoration.• From complete hospitalisation (once discharge criteria have been fulfilled). If additionaleating and behaviour management is necessary, but can be carried out on an outpatientbasis. Also in those cases in which psychopathological intensity requires psychologicaltreatment to modify the patient’s image, beliefs, assertiveness and other aspects relatedwith eating disorders.8.4. In eating disorders, what clinical criteria may beuseful to assess discharge from health care resourcesavailable in the NHS?8.4.1. Criteria for discharge from inpatient care (completehospitalisation)• Normalisation of biological disturbances that have led to complete hospitalisation.• Weight restoration as is established in an individualised programme.• Improved psychopathological state.• Elimination of self-injurious behaviour.• Remission of abnormal eating behaviour and compensatory behaviour.• Improved family conflicts.• Improved general functioning.8.4.2. Criteria for discharge from day patientcare (day hospital)In order to refer to outpatient care (adult or children MHCs):• Weight restoration and/or maintenance as established in the ITP.• Completion of group programmes that had been initiated.• Improved eating pattern and compensatory behaviour (if any).• Improved family conflicts and general functioning that enable outpatient treatment.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS83

For hospital admission:• Weight does not increase as is established in the weight restoration programme.• Does not comply with rules established in the day hospital in terms of meals, physicalactivity restriction and general functioning.• Presence of significant psychopathology.• The patient’s biological state entails a risk of serious complications (heart rate less than45, potassium less than 3.5 mEq/l, hemametesis and rectal bleeding).• At any moment during the patient’s stay at the day hospital, referral to the InternalMedicine Service may be indicated.8.4.3. Criteria for discharge from the outpatient treatmentprogrammeDischarge criteria will depend on the ITP.• Maintenance of non-altered eating behaviour (diets, over-eating and purging) throughouta period of one year.• Maintenance of stable weight that is within normal values throughout a period of one year.• Absence of menstrual irregularities secondary to eating disorders.• Decreased recurrence risk.• Absence of other psychopathological disturbances that require treatment.8.4.4. Discharge criteria for eating disordersThe process will end when clinical improvement is evident and enables the patient to resumenormal daily life, verifying that during a period of time greater than two years the followingcriteria are being fulfilled:• Maintenance of weight and absence of nutritional imbalances.• Absence of eating peculiarities that are harmful to health.• Adequate relational life.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS84

RecommendationsD 8.1. Individuals with eating disorders should be treated in the appropriate care levelbased on clinical criteria: outpatient, day hospital (day care) and general orpsychiatric hospital (inpatient care). (Adapted from recommendation 6.5.8.1 ofthe NICE CPG).D 8.2. Health care professionals without specialist experience in eating disorders orwho are faced with uncertain situations should seek the advice of a trainedspecialist when emergency inpatient care is deemed the most appropriate optionfor a patient with an eating disorder. (Adapted from recommendation 6.5.8.6 ofthe NICE CPG).D 8.3. The majority of patients with BN can be treated on an outpatient basis.Inpatient care is indicated when there is risk of suicide, self-injuries and seriousphysical complications. (Adapted from recommendations 6.5.8.1 and 6.5.8.4 ofthe NICE CPG).D 8.4. Health care professionals should assess patients with eating disorders andosteoporosis and advise them to refrain from performing physical activities thatmay significantly increase the risk of fracture. (Adopted from recommendation6.4.5.3 of the NICE CPG).D 8.5. The paediatrician and the family physician must be in charge of themanagement of eating disorders in children and adolescents. Growth anddevelopment must be closely monitored. (Adapted from recommendation6.4.5.4 of the NICE CPG).D 8.6. Primary care centres should offer monitoring and management of physicalcomplications to patients with chronic AN and repeated therapeutic failureswho do not wish to be treated by mental health services. (Adapted fromrecommendation 5.2.5.8 of the NICE CPG).D 8.7. Family members, especially siblings, should be included in the individualizedtreatment plan (ITP) of children and adolescents with eating disorders. Themost common interventions involve sharing of information, advice onbehavioural management of eating disorders and improving communicationskills. The patient’s motivation to change should be promoted by means offamily intervention. (Adapted from recommendation 6.2.9.13 of the NICECPG).D 8.8. Where inpatient care is required, it should be carried out within a reasonabledistance to the patient’s home to enable the involvement of relatives and carersin treatment, to enable the patient to maintain social and occupational links andto prevent difficulties between care levels. This is particularly important in thetreatment of children and adolescents (Adopted from recommendation 6.5.8.4of the NICE CPG).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS85

D 8.9. Patients with AN whose disorder has not improved with outpatient treatmentmust be referred to day patient treatment or inpatient treatment. For those whopresent a high risk of suicide or serious self-injuries, inpatient management isindicated. (Adapted from recommendation 6.5.8.2 of the NICE CPG).D 8.10. Inpatient management should be considered for patients with AN whose disorderis associated with high or moderate risk due to common disease or physicalcomplications of AN. (Adapted from recommendation 6.5.8.3 of the NICECPG).D 8.11. Patients with AN who require inpatient treatment should be admitted to a centrethat ensures adequate renutrition, avoiding the re-feeding syndrome, with closephysical monitoring (especially in the first few days), along with theappropriate psychological intervention. (Adapted from recommendation 6.5.8.5of the NICE CPG).D 8.12. The family physician and paediatrician should take charge of the assessmentand initial intervention of patients with eating disorders who attend primarycare. (Adapted from recommendation 5.2.5.1 of the NICE CPG).D 8.13. When management is shared between primary and specialized care, thereshould be close collaboration between health care professionals, patients andrelatives and carers. (Adapted from recommendation5.2.5.2 of the NICE CPG). 8.14. Patients with confirmed diagnosis or clear suspicion of an eating disorder willbe referred to different health care resources based on clinical and age criteria. 8.15. Referral to adult and children MHCs by the family physician or paediatricianshould consist of integrated management with shared responsibilities. 8.16. Cases referred to adult of children MHCs still require different levels to worktogether and short- and mid-term monitoring of patients, to avoidcomplications, recurrences and the onset of emotional disorders, and to detectchanges in the patient’s environment that could influence the disease. 8.17. The need to prescribe oestrogen treatment to prevent osteoporosis in girls andadolescents with AN should be carefully assessed, given that this medicationcan hide the presence of amenorrhoea. 8.18. In childhood, specific eating disorder treatment programmes designed for theseages will be required.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS86

9. Treatment of Eating DisordersThe treatment of eating disorders requires multidisciplinary collaboration and can be carried outat different levels of care and health care resources (See Chapter 8, “Interventions at the differentlevels of care”).The objectives of eating disorder treatments are:1. To restore or normalise patient weight and nutritional state to healthy levels in the case ofAN (See question 9.1. of this chapter).Nutritional support can range from a base diet, if the patient presents normonutrition, orspecific diet-therapy (oral diet) if there is an associated pathology, to the administration ofartificial nutrition (enteral oral or parenteral intravenous) if there is severe energetic-proteinmalnutrition.In the outpatient, standard refeeding includes following a normal diet. In day patientmanagement, treatment is more intensive and prolonged than outpatient treatment. Whenoutpatient treatment or day patient treatment is insufficient, or if the patient presents an acuteproblem, inpatient treatment is indicated.2. To treat physical complications. This CPG does not include the specific treatment for allpotential physical complications (See Chapter 4 “Definition and Classification of EatingDisorders”).3. To provide education on healthy, nutritious eating habits. Additionally, generalrecommendations on the principles of a balanced diet with a variety and frequency of foods, ormore specific recommendations based on the type of eating disorder, can be delivered. The aimof nutritional education is to guide the patient and his/her family in terms of the behaviours thatshould be adopted and to increase the patient’s motivation to cooperate and participate intreatment (See Question 9.2. of this chapter).4. To modify/improve prior or acquired dysfunctions due to eating disorders (thoughts,attitudes, inadequate behaviour, etc. 197-199 ), as well as to increase weight, reduce/eliminate bingeeatingand purging, depression, amongst other relevant clinical variables. To this end there areseveral different treatments available:– Psychological therapies (see questions 9.3.-9.8. of this chapter).– Pharmacological treatments (see questions 9.9.-9.15. of this chapter).– Combined interventions (see question 9.16. of this chapter).The therapeutic contract includes ITP (see chapter 8, “Interventions at the different levels ofcare”) and is signed by the patient and the multidisciplinary team of health care professionalsinvolved in the care. This contract ensures that the patient has been informed and that he/she hasaccepted the ITP.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS87

5. To treat associated disorders (comorbidities), both psychiatric (including mooddisturbances, low self-esteem, behaviour, etc.) and physical (diabetes mellitus, etc) (seequestions 9.17 and 9.18 of this chapter).6. To obtain family support for the patient and provide counselling and therapy whennecessary (see chapter 7, “Diagnosis” and question 9.6. in the section “Family therapy”).7. To prevent relapse. This includes addressing and preventing situations that may favourrecurrences and planning strategies to tackle them. Amongst the aspects that should bemanaged, body weight variations, patient requests for diets and drugs, management of propereating habits, engagement in purging behaviour, performance of excessive exercise,management of appropriate ponderal-statural and psychomotor development, detection of anyemotional imbalance or environmental pressure and family management 200, 201 .8. To treat chronic eating disorder cases, as well as the management of eating disorders inspecial situations such as pregnancy and delivery, which are described at the end of this chapter(see questions 9.19 and 9.20 of this chapter, respectively).MEDICAL MEASURESOf all the different interventions or medical measures that can be indicated in the treatment ofeating disorders, only evidence concerning certain types of renutrition (vitamin-mineralsupplements, enteral oral artificial feeding and artificial feeding) and NC has been identified.9.1. Renutrition9.1.1. What is the efficacy of renutrition in patients witheating disorders?Response is based on the NICE CPG (2004) 30 . Two high-quality (1++) SRSE, one elaborated bythe AHRQ of the US (2006) 31 and an additional one by Bulik, et al. (2007) 202 have beenconsidered. The updated search has identified a new RCT (Rigaud, 2007) 203 .Scientific EvidenceIn an RCT (Birmingham, 1994; Canada) 204 a Zn supplement (14 mg/day) was comparedto placebo in a sample of 54 females with AN aged over 15 years. This study yieldspreliminary evidence that Zn can increase the BMI.RCT1+88CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

An RCT (Rigaud, 2007; France) 203 compared enteral feeding (cyclic enteral nutrition)(N=41, 97% women, mean age: 22.5 years) with a control group (N=40, 98% women,mean age: 24.2 years) in a sample of individuals with AN who had been treated for twomonths and with one-year follow-up. When treatment was completed, weight gain was39% greater in the group treated with enteral feeding than in the control group (p

Recommendations(See also recommendations 9.GM.1 to 9.GM.6)D 9.1.1.1. Physical exploration and in some cases treatment with multi-vitamin/mineralsupplements in oral form, both on an outpatient and inpatient basis, isrecommended for patients with AN who are at the stage of body weightrestoration. (Adopted from recommendation 6.4.5.2 of the NICE CPG).D 9.1.1.2. Total parenteral nutrition should not be used for patients with AN unless thepatient refuses nasogastric feeding and/or presents gastrointestinaldysfunction. (Adopted from recommendation 6.4.11.1 of the NICE CPG). 9.1.1.3. Enteral or parenteral renutrition must be applied using strict medical criteriaand its duration will depend on when the patient is able to resume oral feeding.9.1.2. What is the safety of renutrition in patients with AN?The answer is based on the evidence described for renutrition efficacy (question 9.1.1.).Scientific EvidenceIn an RCT no adverse effects were reported. In an RCT (Birmingham, 1994) 204 Noadverse effects were reported. Dropout rate in the group treated with the Zn supplementwas 39% and 32% in the placebo group.RCT1+Summary of the EvidenceCPG 30CPG 30CPG 30There is not sufficient evidence to indicate significant clinical differencesbetween treatment with zinc supplement vs. placebo in the number of adultinpatients with AN who drop out of treatment for any reason (2 RCTs; N= 68;Birmingham, 1994 204 ; Katz, 1987 205 ).There is not sufficient evidence to indicate significant clinical differencesbetween treatment with nasogastric feeding-standard treatment, in the numberof inpatients with AN who drop out of treatment for any reason (1 RCT; Arii,1996 207 ; N=16; RR: 2.33; 95% CI: 0.30 to 17.88).There is limited evidence regarding significant clinical differences betweentotal parenteral nutrition vs. standard treatment in the number of patients withadverse effects (1 RCT; N=22; Pertschuk, 1981) 209 .Recommendations(See recommendations 9.GM.1. to 9.GM.5.)90CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

9.2. Nutritional Counselling (NC)9.2.1. Anorexia nervosa9.2.1.1. What is the efficacy of NC in patients with AN?The answer is based on the NICE CPG (2004) 30 . Two high-quality (1++) SRSE, one elaboratedby the AHRQ of the US (2006) 31 and a more recent one conducted by Bulik, et al. (2007) 202 . Nonew evidence has been identified in the updated search.Scientific EvidenceIn a further RCT (Pike, 2003; USA) 210 , CBT (N=18) was compared to NC (N=15) inwomen (18-45 years) with AN who had been under inpatient treatment for 12months. After weight restoration, a lower percentage of failures, a higher percentageof positive results and a longer time period until recurrence were reported in thegroup that received CBT. However, one of the limitations found in this study was thefact that many patients had received concomitant antidepressant treatment.RCT1+Summary of the EvidenceCPG 30SRSE 311++There is limited evidence to indicate that in inpatients with AN after weightrestoration, CBT is superior to NC in the proportion of recoveries and relapses.(1 RCT; N=33; Pike, 2003) 210 .There is little evidence that CBT is superior to NC in the proportion of patientswho recover and in weight gain.Recommendations(See recommendations 9.GM.1. to 9.GM.5.)9.2.1.2. What is the safety of NC in patients with AN?The answer is based on the evidence described for NC efficacy (question 9.2.1.1.).Scientific EvidenceAN RCT (Pike, 2003) 210 reported an overall dropout rate of 9% (CBT: 0% vs. NC:20%). There was one case of depression and suicidal ideation. The design of thisRCT is limited by the fact that many studied patients were also takingantidepressants, rendering its results questionable.RCT1+91CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Summary of the EvidenceCPG 30There is limited evidence to indicate that CBT is more acceptable than NC ininpatients with AN after weight restoration (1 RCT; N=33; Pike, 2003) 210 ..Recommendations(See recommendations 9.GM.1. to 9.GM.5.)9.2.2. Bulimia nervosa9.2.2.1. What is the efficacy of NC in patients with BN?The answer is based on the NICE CPG (2004) 30 . High-quality (1++) SRSE have also been takeninto account, one elaborated by the AHRQ of the US (2006) 31 and a more recently published oneby Shapiro, et al., . (2007) 211 , which include the same RCT. The updated search has not yieldednew evidence. Results are presented according to the variables studied in the RCT.Variables: reduction/ remission of binge-eating and purging episodesThere is limited evidence to suggest that CBT-BN is more effective than NC in reducingthe frequency of purging episodes by the end of treatment (SMD: -0.95; 95% CI: -1.70 to-0.20) and strong evidence for post-treatment follow-up (SMD: -1.34; 95% CI: -2.13 to -0.55) according to 1 RCT (N=31; Sundgot-Borgen, 2002) 212 .There is no evidence or insufficient evidence to determine that CBT-exposure withresponse prevention (ERP) for binge-eating episodes differs from NC (nutritionaltherapy) in the remission of binge-eating and purging (2 RCTs; N=90; Hsu, 2001 213 ;Jansen, 2002 214 ; RR: 0,82; 95% CI: 0.65 a 1.04) and in the frequency of binge-eating andpurging (1 RCT; N=49; Hsu, 2001 213 ; SMD: 0.43; 95% CI: -0.14 to 0.99) by the end oftreatment.RCT1++RCT1 ++Variables: depression and/or interpersonal and psychosocialfunctioning and/or general psychiatric symptomsThere is no evidence or insufficient evidence to determine that CBT-ERP differs from NC(nutritional therapy) in the scores obtained from the instrument used to assess depression (1RCT; N=49; Hsu, 2001 213 ; SMD: 0.15; 95% CI: -0.41 to 0.72). RCT 1 ++Summary of the EvidenceSRSE 311++If a cognitive component is added to NC (nutritional therapy) its effectivenessimproves (Hsu, 2001) 213 ..92CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Recommendations(See recommendations 9.GM.6. to 9.GM.9.)9.2.2.2. What is the safety of NC in patients with BN?The answer is based on the evidence described for NC efficacy (question9.2.2.1.).Summary of the Evidence1++ There is limited evidence to indicate significant differences between CBT-BNvs. NC in the number of dropouts by the end of treatment (1 RCT; N=31;Sundgot-Borgen, 2002 212 ; SMD: -0.95; 95% CI: -0.70 to -0.20).1++ There is not sufficient evidence of clinically significant differences betweenCBT-ERP and NC (nutritional therapy) in the number of dropouts for anyreason by the end of treatment (2 RCTs; N=90; Hsu, 2001 213 ; Jansen,2002 214 ; RR: 0.95; 95% CI: 0.16 to 5.51).Recommendations(See recommendations 9.GM.6. to 9.GM.9.)CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS93

GENERAL RECOMMENDATIONS ON MEDICALMEASURES FOR EATING DISORDERS(QUESTIONS 9.1-9.2)Eating DisordersRecommendations 9.GM.01. Nutritional support for patients with eating disorders will be selected basedon the patient’s degree of malnutrition and collaboration, and always withthe psychiatrist’s approval. 9.GM.02. Before initiating artificial nutrition the patient’s degree of collaborationmust be assessed and an attempt must always be made to convince him/herof the benefits of natural oral feeding. 9.GM.03. In day hospitals, nutritional support for low-weight patients, where an oraldiet is insufficient, can be supplemented with artificial nutrition (oralenteral nutrition). To ensure its intake, it must be administered during theday hospital’s hours, providing supplementary energy ranging from 300 to1,000 kcal/day. 9.GM.04. Oral nutritional support in eating disorder inpatients is deemed adequate(favourable progress) when a ponderal gain greater than 0.5 kg per week isproduced, with up to 1 kg increments being the usual during that period.Sometimes, when the patient with moderate malnutrition resists resumingnormal feeding, the diet can be reduced by 500-700 kcal and besupplemented by complementary oral enteral nutrition in the same amount,which must be administered after meals and not instead of meals. 9.GM.05. In the case of severe malnutrition, extreme starvation, poor progress orlack of cooperation of the patient in terms of intake, artificial nutritiontreatment is indicated. If possible, an oral diet with or without oral enteralnutrition is always the first step, followed by a 3 to 6 day period to assessthe degree of collaboration and medical-nutritional evolution. 9.GM.06. Regarding estimated energetic requirements, it is recommended thatcaloric needs at the beginning always be below the usual, that realweight, as opposed to ideal weight, be used to make the estimationand that in cases of severe malnutrition energetic requirements be 25to 30 kcal/kg real weight or total kcal not higher than 1,000/day.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS94

Anorexia nervosaRecommendationsD 9.GM.1. In feeding guidelines for children and adolescents with anorexianervosa, carers should be included in any dietary information, educationand meal planning. (Adopted from recommendation 6.5.8.9 of the NICECPG).D 9.GM.2. Feeding against the will of the patient should be used as a last resort in themanagement of AN. (Adopted from recommendation 6.4.13.5 of the NICECPG).D 9.GM.3. Feeding against the will of the patient is an intervention that must beperformed by experts in the management of eating disorders and relatedclinical complications. (Adopted from recommendation 6.4.13.6 of theNICE CPG).D 9.GM.4. Legal requirements must be acknowledged and complied with whendeciding whether to feed a patient against his/her will. (Adopted fromrecommendation 6.4.13.7 of the NICE CPG).D 9.GM.5. Health care professionals must be careful with the healthy weightrestoration process in children and adolescents with AN, administering thenutrients and energy required by providing an adequate diet to promotenormal growth and development. (Adopted from recommendation 6.5.8.8of the NICE CPG).Bulimia nervosaRecommendationsD 9.GM.6. Patients with BN who frequently vomit and abuse laxatives can developabnormalities in electrolyte balance. (Adopted from recommendation7.5.3.1 of the NICE CPG).D 9.GM.7. When electrolyte imbalance is detected, in most cases elimination of thebehaviour that caused it is sufficient to correct the problem. In a smallnumber of cases, oral administration of electrolytes whose plasmatic levelsare insufficient is necessary to restore normal levels, except in casesinvolving gastrointestinal absorption. (Adopted from recommendation7.5.3.2 of the NICE CPG).D 9.GM.8. In the case of laxative misuse, patients with BN must be advised on how todecrease and stop abuse. This process must be carried out gradually.Patients must also be informed that the use of laxatives does not decreasenutrient absorption.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS95

(Adopted from recommendation 7.5.3.3 of the NICE CPG).D 9.GM.9. Patients who vomit habitually must have regular dental check-ups and beprovided with dental hygiene advice. (Adapted from recommendations7.5.3.4 and 7.5.3.5 of the NICE CPG).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS96

PSYCHOLOGICAL THERAPIESIn this section scientific evidence on the efficacy and safety of a series of psychologicaltherapies studied in patients with eating disorders is described. Only randomised controlledtrials (RCT) of sufficient quality have been included. The following therapies have beenassessed: cognitive-behavioural therapy, self-help and guided self-help, interpersonal therapy,family therapy (systemic or unspecified), psychodynamic therapy and behavioural therapy.9.3. Cognitive-Behavioural Therapy (CBT)9.3.1. Anorexia nervosa9.3.1.1. What is the efficacy of CBT in patients with AN?The answer is based on the NICE CPG (2004) 30 . High-quality (1++) SRSE have been taken intoaccount, one elaborated by the AHRQ of the US (2006 31 ) and a further one recently published byBulik, et al. (2007) 202 where the same RCTs are included. The updated search has not yieldedany new evidence.Scientific EvidenceIn an RCT (Channon, 1989; UK 215 ), CBT (N=8; mean age=21.6 years) was compared tobehavioural therapy (BT) (N=8; mean age=24.1 years) and a control group (standardtreatments) (N=8; mean age=25.8 years) in women with AN (mean age range: 21.6-25.8years) treated on an outpatient basis for 12 months. At 6 months of treatment, CBT wasmore effective than BT in improving psychosexual functioning. In contrast, BT wasmore effective than CBT in improving the menstrual cycle. At one year of treatment,BT was more effective than the other two treatments in restoring patients’ weight.In a further RCT (Pike, 2003; USA) 210 , CBT (N=18) was compared to NC (N=15) inwomen (18-45 years) with AN who had been under inpatient treatment for 12 months.After weight restoration, a lower percentage of failures, a higher percentage of positiveresults and a longer period of time until recurrence was reported in the group thatreceived CBT. However, one of the limitations of the study was the fact that manypatients had received concomitant antidepressant treatment.In the third RCT (McInstosh, 2005; New Zealand) 216 , CBT (N=19) was compared to IPT(N=21) and non-specific supportive clinical management (NSCM) (N=16), in women(17-40 years) with AN who were treated on an outpatient basis for 20 weeks. Nonspecificsupportive clinical management (NSCM) was more effective than IPT inimproving patients’ general behaviour and in dietary restraint at 20 weeks of treatmentand was also more effective than CBT in improving general behaviour at 20 weeks.CBT was superior to IPT in improving dietary restraint at 20 weeks.RCT1 +RCT1 +RCT1 +97CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Summary of the Evidence(See also the summary of the evidence for psychological treatment)SRSE 311++SRSE 311++SRSE 311++CPG 30There is little evidence to determine that CBT is more effective than NC in thenumber of patients with AN who recover and in weight gain.CBT did not prove to be more effective than BT or non-specific supportiveclinical management (NSCM) in AN patients’ weight restoration, generalbehaviour and attitudes regarding food. Based on the results, CBT does notexceed IPT.There is not enough evidence to determine that CBT is effective in the acutephase of AN.There is limited evidence to indicate that CBT is more acceptable than NC inAN inpatients after weight restoration (1 RCT; N=33; Pike, 2003) 210 .SRSE 311++CBT treatment can reduce recurrence risk in adults with AN after weightrestoration.Recommendations(See recommendations 9.GP.1. to 9.GP.11.)9.3.1.2. What is the safety of CBT in patients with AN?The answer is based on the evidence pertaining to the question on CBT efficacy (question9.3.1.1.): NICE’s CPG (2004) 30 and 2 high-quality SRSE (1++) (2006) 31 and (2007) 202 . Theupdated search did not yield any new evidence. Question 9.3.1.1. briefly describes the studies.Scientific EvidenceOne of the RCT (Channon, 1989) 215 reported that 13% of patients dropped out oftreatment. Dropouts per groups were: CBT: 0%, BT: 13%, control: 25%; and noadverse effects were reported in any group.In the second RCT (Pike, 2003) 210 , 9% dropped out of treatment (CBT 0%, NC 20%)and depression and suicidal ideations was reported in one case of the CBT group and 3of the NC group.The third RCT (McInstosh, 2005) 216 reported that 38% of studied patients dropped out oftreatment. Dropouts per groups were: CBT 37%, IPT 43%, non-specific supportiveclinical management (NSCM) 31%; however, no adverse effects were reported in anygroup.RCT1 +RCT1 +RCT1 +98CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Summary of the Evidence(See also the summary of the evidence for psychological treatment)CPG 30SRSE 311++There is limited evidence to determine that CBT is more acceptable than NC forAN inpatients after weight restoration (1 RCT; N=33; Pike, 2003) 210 .Psychological interventions do not usually produce adverse effects in treatedpatients.Recommendations(See recommendations 9.GP.1. to 9.GP.11.)9.3.2. Bulimia nervosa9.3.2.1. What is the efficacy of CBT in patients with BN?The source of evidence to answer this question has been NICE’s CPG (2004) 30 , whichdescribes evidence based on outcome variables. It is also based on high-quality (1++) SRSE,one elaborated by the AHRQ of the US (2006) 31 and a further more recent publication byShapiro, et al. (2007) 211 , where six new quality (1++ and 1+) RCT were identified. Theupdated search subsequently yielded two more RCT.Variable: reduction / remission of binge-eating and purgingThere is strong evidence that points to a higher efficacy of CBT-BN vs. wait-list interms of remission in adults with BN by the end of treatment (3 RCTs; N=136;Griffiths, 1994 217 ; Lee, 1986 218 ;Treasure, 1999 219 ; RR: 0,73; 95% CI: 0.61 to 0.88;NNT:4; 95% CI: 3 a 9).There is strong evidence that indicated the efficacy of CBT-BN vs. wait-list in terms ofthe frequency of binge-eating (5 RCTs: N=185; Griffiths, 1994 217 ; Lee, 1986 218 ;Treasure, 1999 219 ; Freeman, 1988 220 ; Wolf, 1992 221 ; SMD: -0.75 95% CI: -1.05 to -0.44)and the frequency of purging in adults by the end of treatment (6 RCTs; N=192;Griffiths, 1994 217 ; Lee, 1986 218 ; Freeman, 1988 220 ; Wolf, 1992 221 ; Agras, 1989 222 ;Leitenberg, 1988 223 ; SMD according to the random effects model: -1.00; 95% CI:-1.63to -0.36).It is not likely that CBT-BN is more effective than BT in reducing the frequency ofbinge-eating (SMD:-0.11; 95% CI:-0.45 to 0.24) and purging episodes by the end oftreatment (SMD: 0.08; 95% CI: -0.27 to 0.42) (3 RCTs; N=131; Fairburn, 1991 224 ;Freeman, 1988 220 ; Wolf, 1992 221 ).There is not sufficient evidence that CBT-BN-ERP is superior to CBT-BN in terms ofremission of binge-eating (2 RCTs; N=53; Cooper, 1995 225 ;Wilson, 1991 226 ; RR: 0.97;RCT1 ++RCT1 ++RCT1 ++RCT1 ++99CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

95% CI: 0.58 to 1.63) and purging (3 RCTs; N=92; Cooper, 1995 225 ;Wilson,1991 226 ;Agras, 1989 222 ; RR: 0.88; 95% CI: 0.62 to 1.24) by the end of treatment.There is sufficient evidence to determine that CBT-BN-ERP is superior to CBT-BNalone in the remission of binge-eating (RR: 1.20; 95% CI: 0.52 to 2.79) and purging(RR: 1.60; 95% CI: 0.76 to 3.36) at follow-up after the end of treatment (1 RCT; N=22;Cooper, 1995) 225 .There is not sufficient evidence to suggest that CBT-BN-ERP treatment is superior toCBT-BN in reducing the frequency of binge-eating (1 RCT; N= 27; Cooper, 1995 225 ;SMD: -0.25 95% CI: -1.01 to 0.50) and purging (3 RCTs: N=83; Agras 2000 227 ;Cooper, 1995 225 , Lenteinberg, 1988 223 ; SMD: -0.17; 95% CI:-0.60 to 0.27) by the end oftreatment.There is not sufficient evidence to suggest that CBT-BN-ERP treatment is superior toCBT-BN in reducing the frequency of purging at follow-up after the end of treatment(2 RCTs; N=48; Cooper, 1995 225 ; Lenteinberg, 1988 223 ; SMD= -0.47; 95% CI: -1.06 to0.11).RCT1 ++RCT1 +RCT1 ++There is limited evidence that indicates that CBT-BN-ERP treatment is superior toCBT-BN in reducing the frequency of purging episodes at follow-up after the end oftreatment (1 RCT; N=25; Wilson, 1991 226 ; SMD: -0.90; 95% CI: -1.73 to -0.07).There is strong evidence that suggests that CBT-BN treatment is more effective thanIPT-BN in the remission of binge-eating (2 RCTs; N=270; Agras, 2000 227 ; Fairburn,1986 228 ; RR: 0.77; 95% CI: 0.67 to 0.87; NNT: 5; 95% CI: 4 a 20) and purging by theend of treatment (1 RCT; N=220; Cooper, 1995 225 ; RR: 0.76; 95% CI: 0.67 to 0,86;NNT: 5; 95% CI: 4 a 8).There is evidence that it is not likely that there are significant differences betweenCBT-BN and IPT-BN treatments in the remission of binge-eating episodes by the endof treatment and at follow-up (2 RCTs; N=270; Agras, 2000 227 ; Fairburn, 1986 228 ; RR:0.93; 95% CI: 0.82 to 1.06).It is not likely that CBT-BN is superior to IPT-BN in reducing the frequency of bingeeating(2 RCTs; N=262;Agras, 2000 227 ; Fairburn, 1986 228 ; SMD: -0.24; 95% CI: -0.48 to0.01) and purging (2 RCTs; N=257; Agras, 2000 227 ; Fairburn, 1986 228 ; SMD: -0.04;95% CI: -0.29 to 0.20) by the end of treatment.There is sufficient evidence that there may be significant differences between CBT-BNvs. PDT in the frequency of binge-eating (1 RCT; N=46; Garner, 1993 229 ; SMD: -0.19;95% CI: -0.77 to 0.39) and purging (1 RCT; N=50; Garner, 1993 229 ; SMD: -0.56; 95%CI: -1.13 to 0.01) by the end of treatment.It is not likely that CBT-BN is superior to FSP (focal supportive psychotherapy) inreducing the frequency of binge-eating (3 RCTs; N=111; Fairburn, 1991 224 ; Freeman,1988 220 ; Wolf, 1992 221 ; SMD: 0.00; 95% CI: -0.37 to 0.38) and purging episodes (4RCTs, N=144; Fairburn, 1991 224 ; Freeman, 1988 220 ; Wolf, 1992 224 , Agras, 2000 227 ;SMD:-0.13; 95% CI: -0.46 to 0.20) by the end of treatment.RCT1 ++RCT1 ++RCT1 ++RCT1 ++RCT1 ++RCT1 ++100CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

There is limited evidence to suggest that CBT-BN is superior to NC in reducing thefrequency of purging episodes at the end of treatment (SMD: -0.95; 95% CI:-1.70 to -0.20) and strong evidence at post-treatment follow-up (SMD:-1.34; 95% CI: -2.13 to -0.55) (one RCT; N=31, Sundgot-Borgen, 2002) 212 .There is not sufficient evidence that CBT-BN differs from GSH (guided self-help) inthe remission of binge-eating and purging episodes at the end of treatment or at posttreatmentfollow-up (RR: 1.63; 95% CI: 0.42 to 6.36) (1 RCT; N=81, Bailer, 2004) 230 .There is limited evidence that CBT-BN differs from GSH in reducing the frequency ofbinge-eating (SMD: 1.20; 95% CI: 0.63 to 1.78) and purging (SMD: 0.55; 95% CI:0.01 to 1.08) by the end of treatment (1 RCT; N=56, Bailer, 2004) 230 .There is not sufficient evidence that CBT-BN differs from GSH in reducing thefrequency of binge-eating (SMD: 0.30; 95% CI: -0.24 to 0.83) and purging (SMD:0.38; 95% CI: -0.15 to 0.92) at post-treatment follow-up (1 RCT; N=55, Bailer,2004) 230 .There is not sufficient evidence that CBT-BN treatment differs from SH (self-help) inthe remission of binge-eating (RR: 0.94; 95% CI: 0.73 to 1.21) and purging (RR: 0.98;95% CI: 0.82 to 6.36) by the end of treatment (1 RCT; N=83, Treasure, 1994) 231 .RCT1 ++RCT1 ++RCT1 ++RCT1 ++RCT1 ++There is evidence that treatment with CBT-BN differs from SH in reducing thefrequency of binge-eating (SMD: 0.03; 95% CI: -0.43 to 0.49) by the end of treatment(1 RCT; N=80, Treasure, 1994) 231 .There is not sufficient evidence that individual CBT differs from group CBT in theremission of binge-eating (RR: 0.83; 95% CI: 0.59 to 1.16) and purging (RR: 0.85;95% CI: 0.57 to 1.27) by the end of treatment (1 RCT; N=60, Chen, 2003) 232 .There is insufficient evidence that individual CBT differs from group CBT in theremission of binge-eating (RR: 0.95; 95% CI: 0.64 to 1) and purging (RR: 1.12; 95%CI: 0.74 to 1.69) at post-treatment follow-up (1 RCT; N=60, Chen, 2003) 232 .There is not sufficient evidence that individual CBT differs from group CBT inreducing the frequency of binge-eating (SMD: -0.18; 95% CI: -0.68 to 0.33) andpurging (SMD: -0.25; 95% CI: -0.76 to 0.26) by the end of treatment (1 RCT; N=60,Chen, 2003) 232 .There is not sufficient evidence that individual CBT differs from group CBT inreducing the frequency of binge-eating (SMD: 0.06; 95% CI: -0.45 to 0.57) andpurging (SMD: 0.08; 95% CI: -0.42 to 0.59) at post-treatment follow-up (1 RCT;N=60, Chen, 2003) 232 .RCT1 ++RCT1 ++RCT1 ++RCT1 ++RCT1 ++101CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Variables: depression and/or interpersonal and psychosocial functioning and/orgeneral psychiatric symptomsThere is strong evidence that points to a higher efficacy of CBT-BN vs. wait-list inreducing depression in adults with BN by the end of treatment (3 RCTs; N=87; Agras,1989 222 ; Lee, 1986 218 ; Leitenberg, 1988 223 ; SMD according to random effects model: -1.19; 95% CI: -1.99 to -0.39).There is not sufficient evidence to determine if CBT-BN differs from BT in reducinggeneral psychiatric symptoms (SMD: -0.26; 95% CI: -0.89 to 0.37) and in interpersonaland psychosocial functioning (SMD: -0.21; 95% CI: -0.84 to 0.42) by the end oftreatment (1 RCT; N=39, Fairburn, 1991) 224 .There is not sufficient evidence that CBT-BN differs from BT in general psychiatricsymptoms (SMD: -0.09; 95% CI: -0.79 to 0.61) and interpersonal and psychosocialfunctioning (SMD: 0.14; 95% CI: -0.56 to 0.85) at follow-up (1 RCT; N=32, Fairburn,1991) 224 .There is insufficient evidence that indicates that CBT-BN differs from PDT ininterpersonal and psychosocial functioning (N=41, SMD: -0.39; 95% CI: -1.01 to 0.23)or in general psychiatric symptoms (N= 48, SMD: -0.60; 95% CI: -1.18 to -0.02) by theend of treatment (1 RCT, Garner, 1993) 229There is no evidence or insufficient evidence to determine that CBT-BN differs fromFSP in interpersonal and psychosocial functioning (SMD: -0.47; 95% CI:-1.28 to 0.34)(1 RCT; N=24, Fairburn, 1986) 228 and in general psychiatric symptoms (2 RCTs; N=69;Fairburn, 1986 228 ; Walsh, 1997 233 ; SMD: -0.29; 95% CI: -0.77 to 0.19) by the end oftreatment or at post-treatment follow-up.There is insufficient evidence that CBT-BN treatment vs. GSH differs in terms ofdepression scores by the end of treatment (SMD: 0.55; 95% CI: 0.02 to 1.09) and atpost-treatment follow-up (SMD: 0.38; 95% CI: -0.15 to0.92) (1 RCT; N=55, Bailer,2004) 230 .RCT1 ++RCT1 ++RCT1 ++RCT1 ++RCT1 ++RCT1 ++There is insufficient evidence that individual CBT differs from group CBT in terms of RCTdepression (SMD: 0.09; 95% CI: -0.41 to 0.60), general psychiatric symptoms (SMD: 1 ++0.07; 95% CI: -0.58 to 0.44) and psychosocial and interpersonal functioning (SMD: -0.16; 95% CI: -0.67 to 0.34) by the end of treatment (1 RCT; N=60, Chen, 2003) 232There is insufficient evidence that individual CBT differs from group CBT in terms ofdepression (SMD: 0.28; 95% CI: -0.23 to 0.l79), general psychiatric symptoms (SMD:0.14; 95% CI: -0.37 to 0.64) and psychosocial and interpersonal functioning (SMD:0.46; 95% CI: -0.05 to 0.98) at post-treatment follow-up (1 RCT; N=60, Chen, 2003) 232 .RCT1 ++Other results102CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

In an RCT (Wilson, 2002; USA) 234 CBT was compared to IPT in a sample of 20 adultwomen with BN under outpatient treatment for 6 weeks. In this study, CBT-BN wassuperior than IPT in reducing dietary restraint at 6 weeks of treatment, improvingbinge-eating and purging at 10 weeks of treatment, and reducing binge-eating aftertreatment. CBT was more effective at reducing the frequency of vomiting at 6 weeksafter treatment than IPT.In an RCT (Wilfley, 1993; USA) 235 that compared group CBT with group IPT andwait-list, in 56 adult women with BN, CBT and IPT were superior to the control group(wait-list) in reducing frequency of binge-eating episodes, disinhibition and restraint at16 weeks of treatment. There were no significant differences between both grouptherapies.A further RCT (Bulik, 1998; New Zealand) 236 performed on 111 adult women withBN under outpatient treatment compared CBT (8 weeks) followed by ERP for bingeeating(G1) with CBT followed by ERP for vomit-inducing signs (G2) and with CBTfollowed by relaxation training (G3). G3 was superior to G1 in reducing depressivebehaviour and body dissatisfaction at the end of treatment and at 2-years follow-up.Relaxation was superior to G2 in reducing depressive behaviour and psychologicaleating disorder and behavioural attitudes at the end of treatment and at 3-years followup.An additional RCT (Sundgot-Borgen, 2002; Norway) 212 compared exercise with CBT,NC, wait-list and healthy control subjects in a group of 74 adult women with BN underoutpatient treatment. Exercise was superior to CBT in reducing binge-eating episodes,laxative abuse and the desire to be thin throughout 18 months of follow-up.An RCT (Bailer, 2004;Austria) 230 compared group CBT with group GSH in 81 adultwomen with BN under outpatient treatment. The GSH was administered bypsychiatrists in training. Both treatments significantly reduced binge-eating, vomiting,laxative abuse, the EDI questionnaire score, the desire to be thin and bodydissatisfaction. At one year follow-up, patients treat with GSH obtained greaterreduction in purging and EDI questionnaire score. CBT was associated with greaterreduction in the desire to be thin at the end of treatment and at follow-up. Boththerapies significantly improved depression at the end of treatment. At follow-up,individuals with GSH obtained better results in decreasing depression scores. Withinthe group of patients who completed treatment, there was a significant difference in thegroup treated with GSH in the maintenance of remission for more than 2 weeks (74%vs. 44%). There were no significant changes in weight in patients treated with GSH.In an RCT (Thiels, 1998;Alemania) 237 CBT was compared to GSH for 16 weeks in agroup of 62 adult women with BN under outpatient treatment. Treatment wasadministered by psychotherapists. In both treatments, a significant decrease in bingeeating,purging and BITE and EAT scores was reported. There were no significantdifferences among groups in terms of depression.In a recent RCT (Schmith, 2007; UK) 238 FT (N=31 BN, N=10 EDNOS) wascompared to CBT-GSH (N=30 BN, N=14 EDNOS) in adolescents aged between 13and 20 years. Treatment was administered for 6 months and follow-up was carried outthroughout 12 months. CBT-GSH reduced binge-eating more than FT at 6 months(p=0.03) although at 12 months the difference between them disappeared. There wereRCT1 +RCT1 +RCT1 ++RCT1 +RCT1 +RCT1 +RCT1 ++103CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

no differences between groups in terms of BMI, diet, eating fast and other behaviouralattitudes related to eating behaviour. The direct cost of treatment was lower for CBT-GSH and no differences were observed in other types of costs.In a recent RCT (Burton, 2007; U.S.) 239 45 women (age range: 14-23 years) fromdifferent educational institutions were recruited. They belonged to different ethnicgroups and social classes and presented depressive symptoms. The group treated withdepression-aimed CBT was compared to a control group (on wait-list). CBT wasadministered for 4 weeks (weekly one-hour sessions) with follow-up at 1 and 6 months.A significant reduction of depressive symptoms was observed in the group treated withCBT, compared to the control (p

SRSE 2401++SRSE 2401++CBT treatment in patients with BN at 6 and 12 months follow-up produced a90% decrease in binge-eating and purging and, at one-year follow-up, 36% ofpatients remitted in terms of binge-eating and purging.Individual and group CBT treatment reduces the main symptoms of BN (bingeeatingand purging) and related short and long-term psychological effects.CPG 30CBT-GSH is superior to FT by reducing binge-eating more rapidly, being lessexpensive and more acceptable for adolescents with BN and/or EDNOS.Further research is necessary to determine if different groups of adolescentsrespond differently to FT and CBT-GSH and which different ways of involvingthe family in treatment can be more or less beneficial (Schmidt, 2007) 238 .RecommendationsA 9.3.2.1.1. CBT-BN is a specifically adapted form of CBT and it is recommended that16 to 20 sessions be performed over 4 or 5 months of treatment. (Adoptedfrom recommendation 7.2.7.3. of the NICE CPG). intervention can beincorporated. (Adopted from recommendation 7.2.7.4. of the NICE CPG).B 9.3.2.1.2.D 9.3.2.1.3.Patients with BN who do not respond to or refuse to receive CBTtreatment may be offered alternative psychological recommendation(Adopted from recommendation 7.2.7.5. of the NICE CPG).Adolescents with BN can be treated with CBT adapted to the their ageneeds, level of development, and, if appropriate, the family’s treatment.(Adopted from recommendation 7.2.7.4. of the NICE CPG).9.3.2.2. What is the safety of CBT in patients with BN?The answer is based on available evidence for CBT efficacy, where studies are briefly described(question 9.3.2.1.).Scientific EvidenceThere is evidence that indicates that CBT treatment dropout is not likely (9RCTs; N=384;Agras, 1989 222 ; Freeman, 1988 220 ; Griffits, 1994 217 ; Lee, 1986 218 ;Leitenberg, 1988 223 ; Wolf, 1992 221 ; Treasure, 1994 231 ; Mitchell, 1990 243 ; Sundgot-Borgen, 2002 212 ; RR: 1.14; 95% CI: 0.74 to 1.74).There is insufficient evidence that there are significant differences between CBT-BNand BT in the number of dropouts by the end of treatment (3 RCT; N=142; Fairburn,1991 224 ; Freeman, 1988 220 ; Wolf, 1992 221 ; RR: 1.20; 95% CI: 0.61 to 2.37).RCT1 ++RCT1 ++105CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

There is insufficient evidence to determine if there are significant differences betweenCBT-BN and CBT-ERP in the number of dropouts by the end of treatment (4 RCTs;N=115;Agras, 1989 222 ; Leitenberg, 1988 223 ; Cooper, 1987 75 ;Wilson, 1991 226 ; RR: 1.14;95% CI: 0.48 to 2.68).There is insufficient evidence to determine if there are significant differences betweenCBT-BN and IPT in the number of dropouts by the end of treatment (2 RCTs; N=70;Agras, 1989 222 ; Fairburn, 1991 224 ; RR: 1.24; 95% CI: 0.84 to 1.83).There is insufficient evidence to determine if there are significant differences betweenCBT-BN and PDT in the number of dropouts by the end of treatment (1 RCT; N=50;Garner, 1993 229 ; RR: 1.00; 95% CI: 0.33 to 3.03).There is insufficient evidence to determine if there are significant differences betweenCBT-BN and FSP in the number of dropouts by the end of treatment (4 RCTs: N=155;Agras, 1989 222 ; Fairburn, 1991 224 ; Freeman, 1988 220 ; Kirckley, 1985 244 ; RR: 0.84; 95%CI: 0.49 to 1.45).There is limited evidence to indicate significant differences between CBT-BN and NCin the number of dropouts by the end of treatment (1 RCT; N=31; Sundgot-Borgen,2002 212 ; SMD: -0.95; 95% CI: -1.70 to -0.20).There is insufficient evidence to determine if there are significant differences betweenCBT-BN and GSH in the number of dropouts by the end of treatment (1 RCT; N=81;Bailer, 2004 230 ; RR: 1.46; 95% CI: 0.75 to 2.86).There is insufficient evidence to determine if there are significant differences betweenCBT-BN and SH in the number of dropouts by the end of treatment (1 RCT; N=83;Treasure, 1994 231 ; RR: 0.98; 95% CI: 0.45 to 2.15).There is insufficient evidence to determine if there are significant differences betweengroup CBT and individual CBT in the number of dropouts by the end of treatment (1RCT; N=60; Chen, 2003 232 ; RR: 1.00; 95% CI: 0.43 to 2.31).In an RCT (Agras, 2000) 227 , the number of dropouts in the CBT group was 28% and24% in the IPT group. There was one case of acute panic attack as an adverse effect inthe CBT group.In another RCT (Wilfley, 1993; USA) 235 , where group CBT was compared to groupIPT and wait-list, in adult females with BN (N=56), the number of dropouts in theCBT group was 14%, 11% in the IPT group and there were no dropouts in the controlgroup (wait-list). No adverse effects were reported.In an RCT (Wilson, 2002) 234 , the total dropout rate by the end of treatment was 30%and 41% at follow-up. No adverse effects were reported.RCT1 ++RCT1 ++RCT1 ++RCT1 ++RCT1 ++RCT1 ++RCT1 ++RCT1 ++RCT1 ++RCT1 +RCT1 +106CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

In an RCT (Bulik, 1998) 236 the overall dropout rate was 17%. Dropouts per groupswere: CBT-ERP for binge-eating: 5%, CBT-ERP for vomit-inducing signs: 6%,relaxation training: 3%. No adverse effects were reported.In an RCT (Sundgot-Borgen, 2002) 212 , after exercise, 20% of dropouts; after CBT,13%; after NC, no dropouts; after wait-list, 6%; after healthy control, 0%. No adverseeffects were reported.In an RCT (Bailer, 2004) 230 , after SH, the dropout rate was 25%; after CBT, dropoutrate was 37%. No adverse effects were reported.In an RCT (Thiels, 1998) 237 , dropout rate in the CBT group was 13%; in GSH, it was29%. No adverse effects were reported.RCT1 ++RCT1 +RCT1+RCT1+Summary of the Evidence(See summary of the evidence for psychological treatment)Recommendations(See recommendations 9.GP.12. and 9.GP.13.)9.3.3. Binge-eating disorder9.3.3.1. What is the efficacy of CBT in patients with BED?The evidence that answers this question in based on the NICE CPG (2004) 30 and on quality RCT(1++ and 1+) that had not been considered in the aforementioned guide but had been included inthe high-quality SRSE, one elaborated by the AHRQ of the US (2006) 31 and a more recentlypublished one conducted by Brownley, et al. (2007) 245 . Three more RCTs have been identifiedin the updated search.Variable: BMIThere is evidence that indicates it is not likely that there is a clinicallysignificant difference between CBT-BED and wait-list in body weightmodification by the end of treatment (BMI when possible) (3 RCTs;N=176;Agras, 1995 246 ; Gorin, 2001 247 ; Telch, 1990 248 ; SMD: -0.02; 95% CI: -0.33to 0.30).RCT1++107CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

There is evidence that indicates it is not likely that there is a clinically significantdifference between CBT-BED and IPT-BED in body weight modification by the end oftreatment (BMI when possible) (1 RCT; N=158; Wilfley, 2002 249 ; SMD: 0.06; 95% CI:-0.26 to 0.37).There is insufficient evidence to determine that there are significant differencesbetween BCT-BED and behavioural weight control (BWC) in the variation of bodyweight (BMI when possible) by the end of treatment (SMD: 0.24; 95% CI: -0.41 to0.90) and at follow-up (SMD: 0.05; 95% CI: -0.60 to 0.70) (1 RCT; N=37, Nauta,2000) 250 .RCT1++RCT1++Variables: reduction / remission of binge-eating and purgingThere is strong evidence that CBT-BED is more effective than being on wait-list interms of significant remission of binge-eating (4 RCT; N=226; Agras, 1995 246 ; Gorin,2001 247 ; Telch, 1990 248 ; Wilfley, 1993 235 ; based on random effects model RR:0.64; 95%CI: 0.49 to 0.84; NNT: 3; 95% CI: 2 to 7) and reduction of binge-eating episodes (4RCTs: N=214;Agras, 1995 246 ; Gorin, 2001 247 ;Telch, 1990 248 ;Wilfley, 1993 235 ; randomeffects model SMD: -1.30; 95% CI: -2.13 to -0.48) by the end of treatment.There is evidence that indicates it is not likely that there is a significant difference in thereduction of binge-eating frequency between CBT-BED and IPT-BED, by the end oftreatment (2 RCT: N=194; Wilfley, 1993 235 and 2002 249 ; SMD:-0.07; 95% CI: -0.35 to0.22) and at post-treatment follow-up (1 RCT; N=138; Wilfley, 2002 249 ; SMD: 0.14;95% CI: -0.19 to 0.48).There is strong evidence that indicates a significant difference in binge-eating remissionin favour of CBT-BED vs. BWC at post-treatment follow-up (1 RCT; N=37; Nauta,2000 250 ; RR: 0.25; 95% CI: 0.08 to 0.79; NNT: 3; 95% CI: 2 to 8).RCT1++RCT1++RCT1++Variables: depression and/or interpersonal and psychosocial functioning and/orgeneral psychiatric symptomsEvidence indicates that it is unlikely to be a significant difference betweenCBT-BED and the control group (wait-list) in depression scores by the end oftreatment (4 RCTs; N=214; Agras, 1995 246 ; Gorin, 2001 247 ; Telch, 1990 248 ;Wilfley, 1993 235 ; SMD: -0.18; 95% CI: -0.46 to 0.10).There is insufficient evidence to indicate that there are significant differences betweenCBT-BED and the control group (wait-list) in general psychiatric scores (1 RCT; N=42;Agras, 1995 246 ; SMD: 0.00; 95% CI: -0.69 to 0.69) and in interpersonal andpsychosocial functioning (2 RCTs; N=194; Agras, 1995 246 ; Wilfley, 1993 235 ; SMD: 0.22;95% CI: -0.06 to 0.50) by the end of treatment.RCT1++RCT1++108CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Evidence indicates that it is unlikely to be a significant difference between CBT-BEDand IPT-BED in depression scores by the end of treatment (2 RCTs; N=194; Wilfley,1993 235 y 2002 249 ; DME; 0,22; 95% CI: -0,06 a 0,50) and at post-treatment follow-up (1RCT; N=138; Wilfley, 2002 249 ; SMD:0.10; 95% CI: -0.24 to 0.43).Evidence indicates that it is unlikely to be a significant difference between CBT-BEDand IPT-BED in psychosocial / interpersonal functioning by the end of treatment (2RCTs: N=194; Wilfley, 1993 235 and 2002 249 ; SMD: 0.06; 95% CI: -0.22 to 0.35).Evidence indicates that it is unlikely to be a significant difference between CBT-BEDand IPT-BED in depression scores at post-treatment follow-up (1 RCT, Wilfley,2002 249 : N=138; SMD: 0.13; 95% CI:-0.20 to 0.47).Evidence indicates that it is unlikely to be significant differences between CBT-BEDand BWC in depression scores by the end of treatment (SMD:-0.31; 95% CI:, -0.97 to0.34) and at follow-up (SMD: 0.21; 95% CI: -0.45 to 0.86) (1 RCT; N=37, Nauta,2000) 250 .RCT1++RCT1++RCT1++RCT1++Other resultsIn an RCT (Gorin, 2003; USA) 251 group CBT was compared to CBT with partnerinvolvement and wait-list, in a group of 94 adult women with BED under outpatienttreatment over 12 months. Compared to the control subjects, both groups significantlyreduced binge-eating and BMI, and improved psychological results such asdisinhibition, depression and self-esteem. The partner’s involvement in therapy did notproduce significant improvement compared to normal CBT. Both group therapies havesignificantly reduced depression scores compared to the control group, but there are nodifferences between them. Average BMI decrease from baseline to follow-up was 0.11for CBT and 0.77 for CBT-partner. This suggests that CBT alone does not produce asignificant change in BMI.In an RCT (Hilbert, 2004; Germany) 252 CBT-body exposure component was comparedto CBT-cognitive interventions for image disturbance in 28 adult women with BEDunder outpatient treatment with at least one binge-eating episode per week for 4months. Treatment duration was 5 months. Both groups decreased binge-eating anddepression scores but there were no significant differences between them.In a recent RCT (Schmith, 2007; UK) 238 FT was compared (N=31 BN, N=10 EDNOS)with CBT-GSH (N=30 BN, N=14 EDNOS) in adolescents between the ages of 13 and 20years, with BN or EDNOS. Treatment was administered over 6 months with 12-monthfollow-up. CBT-GSH was more effective at reducing binge-eating at 6 months than FT(p=0.03) even though this difference disappeared at 12 months. There were nodifferences between groups in terms of BMI, diet, eating fast and other attitudinal eatingdisorder symptoms. The direct cost of treatment was lower for CBT-GSH and noRCT1+RCT1+RCT1++109CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

differences were observed in other types of costs. CBT-GSH is slightly superior to FTin reducing binge-eating more quickly, being less costly and presenting betteracceptability for adolescents with BN and/or EDNOS.An RCT (Munsch, 2007; Switzerland) 253 in 80 participants (88.85% women, age 18-70years) diagnosed with BED compared CBT (N=44) to behavioural weight losstreatment (BWLT) (N=36) in 16 weekly sessions with 12-month follow-up. CBT wassignificantly more effective at reducing BMI (p27 kg/m 2 ) and regular access to a computer were included,group CBT (N=22; 90-minute sessions in groups of 5 to 10 people) was compared to CBT-CD(N=22; CBT using CD-ROM for treatment of obesity and eating behaviour that affects health)and to waiting list (N=22). Treatment duration was 10 weeks.Treatment acceptability was measured using debilitation of individuals who had beenoriginally assigned to the waiting list group after changing from one treatment toanother. The majority of patients on waiting list preferred to receive the CD-ROM thangroup CBT when their waiting time ended. There is a significant difference in bothgroups compared to the control group in reducing the number of daily binge-eatingepisodes.RCT1++Summary of the EvidenceSRSE 311++SRSE 311++SRSE 311++CBT is more effective at reducing the frequency of binge-eating episodes andincreasing their remission. Both individual and group CBT, when compared toother interventions carried out in the control group, obtain better results inachieving abstinence and its maintenance over the 4 months followingtreatment (Hilbert, 2004 252 ; Gorin, 2003 251 ). CBT is not associated with weightloss.CBT also improved psychological aspects (disinhibition, etc.) (Hilbert, 2004 252 ;Gorin, 2003 251 ).The efficacy of CBT in reducing body weight in BED patients is not adequatelydocumented (Hilbert, 2004 254 ; Gorin, 2003 251 ).Recommendations(See also recommendations 9.GP.14. and 9.GP.17.)110CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

A 9.3.3.1. Adult patients with BED can be offered a specifically adapted form ofCBT. (Adopted from recommendation 8.2.7.4. of the NICE CPG).9.3.3.2. What is the safety of CBT in patients with BED?The answer is based on the evidence described for CBT efficacy where studies are brieflydescribed (question 9.3.3.1.): in the NICE CPG (2004) 30 and in two quality RCT (1++ and 1+)that were not considered in the aforementioned guide but were included in the high-qualitySRSE (1++) published in the years 2006 31 and 2007 245 . The updated search has identified onemore RCT. Question 9.3.3.1. briefly describes the studies.Scientific EvidenceThere is limited evidence to indicate that there are significant differences between CBTand waiting list in the number of dropouts for any reason by the end of treatment (4RCTs; N=222;Agras, 1995 246 ; Gorin, 2001 247 ,Telch, 1990 248 ,Wilfley, 1993 235 ; RR:1.86;95% CI: 1.10 to 3.15; NNT: 7; 95% CI: 4 to 34).There is not sufficient evidence to indicate that there are significant differencesbetween CBT and IPT in the number of dropouts for any reason by the end of treatment(2 RCTs; N=198; Wilfley, 1993 235 and 2002 249 ; RR: 1.89; 95% CI: 0.89 to 4.02).There is insufficient evidence to indicate that there are significant differences betweenCBT and BWC in the number of dropouts for any reason by the end of treatment (1RCT; N=37: Nauta, 2000 250 ; RR: 0.76; 95% CI: 0.18 to 3.29).The RCT (Hilbert, 2004 252 ; Gorin, 2003 251 ; Peterson, 2001 255 and 1998 256 ) did not reportany adverse effects. The overall dropout rate in one of the RCT (Gorin, 2003) 251 was34% and, in another RCT (Hilbert, 2004) 252 , 14% in each treatment group.In an RCT (Shapiro, 2007) 254 that compared group CBT to CBT-CDROM and wait-list,dropouts in each group were as follows: CD-ROM 32%; group CBT 41%; and wait-list9%. The CBT-CD programme has better acceptability than group CBT in patients withBED.RCT1+RCT1+RCT1+RCT1+RCT1++Summary of the Evidence(See summary of the evidence for psychological treatment)Recommendations(See recommendations 9.GP.12. and 9.GP.17.)111CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

9.4. Self-Help (SH) and Guided Self-Help (GSH)9.4.1. Bulimia nervosa9.4.1.1. What is the efficacy of SH and GSH in patients with BN?The answer to this question is based on the NICE CPG (2004) 30 and on three high-quality SRSE(1++): the one elaborated by the AHRQ 31 , one Cochrane review 257 and a more recent publicationby Shapiro, et al. (2007) 211 . The updated search has not yielded any new evidence.Variables: reduction / remission of binge-eating and purgingEvidence indicates that it is unlikely to be a clinically significant difference between SHand the control group (wait-list) in binge-eating (2 RCTs; N=139; Treasure, 1994 231 ;Carter, 2003 242 ; RR: 0.96; 95% CI: 0.85 to 1.09) and purging (2 RCTs;N=139;Treasure, 1994 231 ; Carter, 2003 242 ; RR: 0.97; 95% CI:0.87 to 1.07) remission bythe end of treatment.There is not sufficient evidence to indicate clinically significant differences between SHand the control group (wait-list) in the frequency of binge-eating episodes by the end oftreatment (1 RCT; N=39; Mitchel, 2001 258 ; SMD: 0.48; 95% CI: -0.16 to 1.12).RCT1++RCT1++Variables: depression and/or interpersonal and psychosocial functioning and/orgeneral psychiatric symptomsThere is not sufficient evidence to indicate clinically significant differences betweenSH and wait-list in depression scores by the end of treatment. (1 RCT, N=57; Carter,2003 242 ; SMD: 0.47; 95% CI: -0.06 to 1.00).There is not sufficient evidence to indicate clinically significant differences betweenSH and wait-list in psychosocial interpersonal function by the end of treatment (1 RCT,N=57; Carter, 2003 242 ; SMD: 0.15; 95% CI: -0.37 to 0.67).RCT1++RCT1++Other resultsIn an RCT (Durand y King, 2003) 259 in a sample of 68 patients, GSH administered by ageneral practitioner was compared to clinical treatment administered by a specialist.Treatment duration was determined by the clinician. Both groups of patients reporteddecreased BITE and EDE scores. However, binge-eating and purging behaviours didnot significantly decrease. Depression symptoms decreased in a similar fashion in bothgroups. No weight changes were observed in any of the groups.RCT1+112CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

In an RCT (Carter, 2003; Canada) 242 the SH-based CBT manual specifically gearedtowards eating disorders was compared to SH with a self-affirmation manual (nonspecific)and to wait-list in 85 adult women with BN under outpatient treatment. Theindividuals who provided guidance were non-specialised facilitators without clinicaltraining. Both SH therapies significantly reduced binge-eating and purging behaviourswhen compared to waiting (wait-list). SH-based CBT was associated with a greaterreduction of excessive exercise compared to the control group (on wait-list) and nonspecificSH.RCT1+Summary of the EvidenceSRSE 311++SRSE 2571++SRSE 2571++Four RCTs provide evidence of the efficacy of SH in BN. There are nodifferences in efficacy between the different types of SH (Carter, 2003) 242 .There is preliminary evidence that indicates that general practitioners can carryout SH treatment. (Durand and King, 2003) 259 .Due to the fact that SH and GSH treatments for BN, when compared to thecontrol group (patients on wait-list or receiving standard treatment), produce ashort-term reduction of eating disorder severity and other symptoms, theseprocedures seem useful as the first step of treatment. It is yet unclear ifguidance is necessary, how much of it and who should provide it. Patientpreference and availability of resources must be taken into account.No significant differences were found in any of the results when SH, GSH andformal psychological therapy administered by a therapist were compared, eventhough it is probable that these analyses do not have sufficient statistical power.However, it is suggested that SH treatments possibly be considered analternative to treatments administered by a specialised therapist, taking both thepatient’s preference and availability of resources into consideration.RecommendationsB 9.4.1.1.1. A possible first step in BN treatment is encouraging patients to initiate aSH programme (guided or not). (Adapted from recommendation 7.2.7.1.of the NICE CPG).B 9.4.1.1.2. SH (guided or not) is sufficient treatment for a limited number of patientswith BN. (Adapted from recommendation 7.2.7.2. of the NICE CPG).9.4.1.2. What is the safety of SH and GSH in patients with BN?The answer in based on the NICE CPG (2004) 30 and on high-quality SRSE (1++) published in2006 31 and 2007 211 . The updated search has not yielded any new evidence. Studies are brieflydescribed in question 9.4.1.1.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS113

Scientific EvidenceThere is insufficient evidence to indicate clinically significant differences between SHand wait-list in the number of dropouts for any reason by the end of treatment (3 RCTs,N=183; Carter, 2003 242 ; Mitchel, 2001 258 ; Treasure, 1994 231 ; RR: 0.68; 95% CI: 0.38 to1.19).There is insufficient evidence to indicate clinically significant differences between GSHand wait-list in the number of dropouts for any reason by the end of treatment (1 RCT;N=47;Walsh, 2004 328 ; RR: 1.38; 95% CI: 0.98 to 1.96).In an RCT (Durand and King, 2003 259 ), the overall dropout rate was 21%. Dropouts pergroups were: SH by family physician, 24%; specialist treatment, 18%. No adverseeffects were reported.In an RCT (Carter, 2003) 242 the dropout rate in the CBT manual group was 18%; nonspecifictreatment, 25%; wait-list, 28%. No adverse effects were reported.RCT1+RCT1+RCT1+RCT1+Summary of the Evidence(See summary of the evidence for psychological treatment)Recommendations(See recommendations 9.GP.12 to 9.GP.17)9.4.2. Binge-Eating Disorder9.4.2.1. What is the efficacy of SH and GSH in patients with BED?The answer is based on the NICE CPG (2004) 30 and on three high-quality SRSE (1++): the oneelaborated by the AHRQ 31 , a Cochrane 257 review and a more recently published one by Brownley,et al., 2007 245 . The updated search has not yielded any new evidence.Variable: BMIThere is insufficient evidence to determine that there are clinically significantdifferences between SH and GSH in mean BMI by the end of treatment (2 RCTs,N=109; Loeb 2000 260 ; Carter, 1998 262 ; SMD: 0.08; 95% CI: -0.30 to 0.46) and at followup(1 RCT, N=69; Carter, 1998 262 ; SMD: 0.19; 95% CI: -0.29 to 0.66).RCT1++114CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Variable: reduction / remission of binge-eating and purgingThere is insufficient evidence to determine that there are clinically significantdifferences between SH and GSH in the remission of binge-eating by the end oftreatment (1 RCT, N=40; Loeb, 2000 260 ; RR: 0.71; 95% CI: 0.42 to1.21).There is limited evidence to determine that GSH is superior to SH in reducing thefrequency of binge-eating by the end of treatment (2 RCTs, N=109; Loeb, 2000 260 ;Carter,1998 261 ; SMD: -0.48; 95% CI: -0.86 to -0.09).There is insufficient evidence to determine that there are clinically significantdifferences between SH and GSH in the frequency of binge-eating at post-treatmentfollow-up (1 RCT, N=69; Carter, 1998 261 ; SMD: -0.24; 95% CI: -0.71 to 0.23).RCT1++RCT1++RCT1++Variables: depression and/or interpersonal and psychosocial functioning and/orgeneral psychiatric symptomsThere is insufficient evidence to determine that there are clinically significantdifferences between SH and GSH in depression scores by the end of treatment (1 RCT,N=40; Loeb, 2000 260 ; SMD: -0.22; 95% CI: -0.85 to 0.40).There is insufficient evidence to determine that there are clinically significantdifferences between SH and GSH in general psychiatric symptoms by the end oftreatment (2 RCTs, N=109; Loeb, 2000 260 ; Carter, 1998 261 ; SMD: -0.18; 95% CI: -0.55to 0.20) and at follow-up (1 RCT, N=69; Carter, 1998 261 ; SMD: -0.20; 95% CI: -0.68 to0.27).RCT1++RCT1++More resultsIn an RCT (Peterson, 1998; USA 256 ) SH administered by a therapist (G1) was comparedto partial SH (G2), structured SH (G3) and wait-list (G4) in 61 patients with BED. G1used group discussion and the psychoeducational component; in G2, participantswatched a 30-minute psychoeducational video and later engaged in a group discussionwith the therapist, and in G3 participants watched the 30-minute video and discussed itamongst themselves. All treated groups obtained better results than the control group inremission and frequency of binge-eating and symptoms related with eating disorders.Abstinence proportion (complete remission) was 68% to 87% in the treated groups and12.5% in the control group. There were no differences amongst groups in terms ofdepression and BMI.In an RCT (Peterson, 2001; USA) 255 SH administered by a therapist (G1) was comparedto partial SH (G2) and structured SH (G3) in 61 patients with BED. The three groupsshowed significant improvement in remission, binge-eating frequency and bodydissatisfaction. The SH group obtained greater remission by the end of treatment, butnot at follow-up. There were no differences amongst groups in terms of depression andBMI.RCT1+RCT1+115CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Summary of the EvidenceSRSE 311++SRSE 2571++SRSE 2571++SH and GSH are efficacious in reducing binge-eating remission and frequencyand psychological traits associated with eating disorders. This therapy obtainssimilar values to those obtained in trials that use face-to-face psychotherapy in ashort period of time. There are no changes in depression and BMI.Given that SH and GSH treatments for BED, when compared to controls (onwait-list or receiving standard treatment), produce a short-term reduction ofeating disorder severity and other symptoms, these procedures seem useful as afirst step of treatment. It remains unclear if guidance is necessary, how much ofit and who should provide it. Patient preference and availability of resourcesshould be taken into consideration.No significant differences were found in several results pertaining to SH andGSH interventions and formal psychological therapy administered by atherapist, even though it is probable that these analyses do not have sufficientstatistical power. However, it is suggested that SH treatment possibly beconsidered an alternative to treatments administered by a specialised therapist,taking both patient preference and availability of resources into account.Recommendations(See recommendations 9.GP.12. to 9.GP.17.)9.4.2.2. What is the safety of SH and GSH in patients with BED?The answer is based on the NICE CPG (2004) 30 and on the high-quality (1++) SRSE of theAHRQ and a more recent one conducted by Brownley, et al., 2007 211 . The updated search has notyielded any new evidence. Studies are briefly described in question 9.4.2.1.Scientific EvidenceThere is insufficient evidence to determine that there are significant differencesbetween SH and GSH in the number of dropouts for any reason by the end of treatment(1 RCT, Loeb, 2000 260 ; N=40; RR: 0.86; 95% CI; 0.35 to 2.10).RCT1++In an RCT (Peterson, 1998) 256 , the overall dropout rate was 16%. Dropouts per groupswere: G1: 13%, G2: 11%, G3: 27% and G4: 0%. No adverse effects were reported.Another RCT (Peterson, 2001 255 ), reported an overall dropout rate of 14%. No adverseeffects were reported.RCT1++RCT1+116CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

In yet another RCT (Carter, 1998 261 ), the overall dropout rate was 12%. Dropouts pergroups were: GSH: 24%, SH: 0% and wait-list: 4%. No adverse effects were reported.RCT1+Recommendations(See recommendations 9.GP.12. to 9.GP.14.)9.5. Interpersonal Therapy (IPT)9.5.1. Anorexia nervosa9.5.1.1. What is the efficacy of IPT in patients with AN?The answer is based on a high-quality SRSE (1++) elaborated by the AHRQ of the US (2006) 31 .The results of the previous SRSE are maintained in a further high-quality (1++) SRSE based onthe same RCT published one year later (Bulik, et al., 2007) 202 . The updated search has notyielded any new RCTs.Scientific EvidenceIn an RCT (McInstosh, 2005; New Zealand) 216 CBT (N=19) was compared to IPT(N=21) and to non-specific supportive clinical management (NSCM) (N=16) in women(17-40 years) with AN and low weight who were treated on an outpatient basis over 20weeks. NSCM was superior to IPT in improving the general functioning of patients andin dietary restraint at 20 weeks of treatment; NSCM was superior to CBT in improvinggeneral functioning at 20 weeks, and CBT was superior to IPT in improving dietaryrestraint at 20 weeks.RCT1+Summary of the Evidence(See summary of the evidence for psychological treatment)Recommendations(See recommendations 9.GP.1. to 9.GP.11.)9.5.1.2. What is the safety of IPT in patients with AN?The answer is based on two high-quality SRSE (1++) described in the question regarding IPTefficacy 31, 202 .CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS117

Scientific EvidenceIn an RCT (McInstosh, 2005) 216 , there was an overall dropout rate of 38% in the grouptreated with IPT. No adverse effects were reported.RCT1+Summary of the Evidence(See summary of the evidence for psychological treatment)Recommendations(See recommendations 9.GP.1. to 9.GP.11.)9.5.2. Bulimia nervosa9.5.2.1. What is the efficacy of IPT in patients with BN?The evidence for this question is based on the NICE CPG (2004) 30 , where RCTs aredescribed in terms of outcome variables, and on the high-quality (1++) SRSE elaborated by theAHRQ of the US (2006) 31 and a more recent high-quality (1++) one published by Shapiro, et al.(2007) 211 . The updated search has not yielded any new evidence.Variable: reduction / remission of binge-eating and purgingThere is strong evidence that suggests that CBT-BN treatment is more effective thanIPT-BN in the remission of binge-eating (2 RCTs; N=270; Agras, 2000 227 ; Fairburn,1986 228 ; RR: 0.77; 95% CI: 0.67 to 0.87; NNT: 5; 95% CI: 4 to 20) and purging by theend of treatment (1 RCT; N=220; Cooper, 1995 225 ; RR: 0.76; 95% CI: 0.67 to 0.86;NNT: 5; 95% CI: 4 to 8).RCT1 ++There is evidence that indicates that there are no significant differences between CBT-BN and IPT-BN in the remission of binge-eating at post-treatment follow-up (2 RCTs;N=270; Agras, 2000 227 ; Fairburn, 1986 228 ; RR: 0.93; 95% CI: 0.82 to 1.06).RCT1 ++It is not likely that CBT-BN is superior to IPT-BN in reducing the frequency of bingeeating(2 RCTs; N=262;Agras, 2000 227 ; Fairburn, 1986 228 ; SMD: -0.24; 95% CI: -0.48 to0.01) and purging (2 RCTs; N=257; Agras, 2000 227 ; Fairburn, 1986 228 ; SMD: -0.04; 95%CI: -0.29 to 0.20) by the end of treatment.RCT1 ++Variables: depression and/or interpersonal and psychosocial functioningand/or general psychiatric symptomsThere is insufficient evidence to determine that there are significant differencesbetween CBT and IPT in general psychiatric symptom scores by the end of treatmentRCT 1++118CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Scientific EvidenceThere is insufficient evidence to determine if there are significant differences betweenCBT-BN and IPT in the number of dropouts by the end of treatment (2 RCTs; N=270;Agras, 1989 222 ; Fairburn ,1991 224 ; RR: 1.24; 95% CI: 0.84 to 1.83).RCT1 ++One RCT (Wilson, 2002) 234 claimed that the overall dropout rate by the end oftreatment was 30% and 41% at follow-up. No adverse effects were reportedOne RCT (Wilfley, 1993; USA) 235 compared group CBT to group IPT and to wait-listin 56 adult women with BN. Overall dropout rate was 14% (CBT: 33%, IPT: 11%,and on wait-list: 0%). No adverse effects were reported.RCT1 +RCT1 ++Summary of the Evidence(See summary of the evidence for psychological treatment)Recommendations(See recommendations 9.GP.12 to 9.GP.17)9.5.3. Binge-Eating Disorder9.5.3.1. What is the efficacy of IPT in patients with BED?Evidence is derived from the NICE CPG (2004) 30 where outcome variables are described andfrom high-quality SRSE (1++) elaborated by AHRQ of the US (2006) 31 and by Brownley, et al.(2007) 245 . The updated search has not yielded any new evidence.Variable: BMIThere is evidence that indicates is not likely that there is a clinically significantdifference between CBT-BED and IPT-BED in body weight variation by the end oftreatment (BMI when possible) (1 RCT, N=158; Wilfley, 2002 234 ; SMD: 0.06; 95% CI:-0.26 to 0.37).RCT1 ++Variables: reduction / remission of binge-eating and purgingThere is evidence that indicates it is not likely that there is a significant differencebetween CBT-BED and IPT-BED in the reduction of binge-eating frequency by the endof treatment (2 RCTs; N=194; Wilfley, 1993 235 and 2002 234 ; SMD: -0.07; 95% CI: -0.35RCT1 ++120CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

to -0.22) and at post-treatment follow-up (2 RCTs; N=138; Wilfley, 1993 235 and 2002 234 ;SMD: 0.14; 95% CI: -0.19 to 0.48).There is strong evidence that suggests there is a clinically significant differencebetween IPT-BED and wait-list in the remission of binge-eating (2 RCTs; N=38;Wilfley, 1993 235 and 2002 234 ; RR: 0.56; 95% CI: 0.37 to 0.84; NNT: 3; 95% CI: 2 to 5)and in the reduction of binge-eating frequency by the end of treatment (2 RCTs; N=38;Wilfley, 1993 235 and 2002 234 ; SMD: -1.44; 95% CI: -2.16 to -0.72).RCT1 ++Variables: depression and/or interpersonal and psychosocial functioning and/orgeneral psychiatric symptomsThere is limited evidence that suggests a clinically significant difference between IPT-BED and wait-list in improving depression scores by the end of treatment (2 RCTs;N=38; Wilfley, 1993 235 and 2002 234 ; SMD: -0.80; 95% CI:-1.46 to -0.13).RCT1 ++There is insufficient evidence to suggest that there is a clinically significant differencebetween IPT-BED and wait-list in improving interpersonal and psychosocialfunctioning by the end of treatment (2 RCTs; N=38; Wilfley, 1993 235 and 2002 234 ; SMD:0.00; 95% CI: -0.64 to -0.64).RCT1 ++There is evidence that indicates it is not likely that there is a significant differencebetween CBT-BED and IPT-BED in depression scores by the end of treatment (2RCTs; N=194; Wilfley, 1993 235 and 2002 234 ; SMD: 0.22; 95% CI: -0.06 to 0.50) and atpost-treatment follow-up (1 RCT; N=138; Wilfley, 2002 234 ; SMD:0.10; 95% CI: -0.24to 0.43).RCT1 ++There is evidence that indicates it is not likely that there is a significant differencebetween CBT-BED and IPT-BED in psychosocial and interpersonal functioning by theend of treatment (2 RCTs, N=194; Wilfley, 1993 235 and 2002 234 ; SMD: 0.06; 95% CI: -0.22 to 0.35).RCT1 ++There is evidence that indicates it is not likely that there is a significant differencebetween CBT-BED and IPT-BED in mean depression scores at post-treatment followup(1 RCT; Wilfley, 2002 234 ; N=138; SMD: 0.13; 95% CI:-0.20 to 0.47).RCT1 ++Summary of the Evidence(See summary of the evidence for psychological treatment)121CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Recommendations(See also recommendations 9.GP.12. to 9.GP.17.)B 9.5.3.1. IPT-BED can be offered to patients with persistent BED (adapted fromrecommendation 8.2.7.5. of the NICE CPG).9.5.3.2. What is the safety of interpersonal therapy in patients withBED?The evidence derives from the NICE CPG (2004) 30 and high-quality SRSE 31, 245 . The updatedsearch has not yielded any new evidence. Studies are briefly described in question 9.5.3.1.Scientific EvidenceThere is insufficient evidence to determine that there are significant differencesbetween CBT and IPT in the number of dropouts for any reason by the end of treatment(2 RCTs; N=198; Wilfley, 1993 235 and 2002 234 ; RR: 1.89; 95% CI: 0.89 to 4.02).RCT1 +In an RCT (Wilfley, 2002) 234 , dropout rate for CBT was 20% and 16% for IPT. Noadverse effects were reported.RCT1 +Summary of the Evidence(See summary of the evidence for psychological treatment)Recommendations(See recommendations 9.GP.12. to 9.GP.17.)9.6. Family Therapy (FT) (systemic or unspecified)9.6.1. Anorexia nervosa9.6.1.1. What is the efficacy of FT (systemic) in patients with AN?The answer is based on the NICE CPG (2004) 30 and on the high-quality SRSE (1++) elaboratedby the AHRQ of the US (2006) 31 and a more recently published SRSE (Bulik, et al., 2007) 202 . Theupdated search has not yielded any new evidence on FT.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS122

Scientific EvidenceIn an RCT (Crisp, 1991; UK) 263 in adult women with AN the following treatments werecompared: G1) in inpatients: individual therapy-FT-group therapy-NC-occupationaltherapy (N=30); G2) in outpatients: individual psychological therapy-FT-NC (N=20);G3) in outpatients: group FT-NC (N=20); G4) control group (N=20). A two-yearfollow-up was conducted. Individual therapy and FT in outpatients is more effectivefor weight restoration at one or two years of follow-up. FT in adults with AN issuperior to standard treatments in increasing BMI, restoring menstruation and reducingbulimic symptoms.RCT1 +In an RCT (Dare, 2001; UK) 264 FT was compared to cognitive analytical therapy, focalsupportive psychotherapy (FSP) and standard treatments in adult patients with AN(98% women) under outpatient treatment. At one-year follow-up, FT and FSP wereassociated with increased weight gain and a greater proportion of patients who hadrecovered or showed significant improvement.RCT1 +In two RCTs (Russel, 1987; UK 265 ; Eisler, 1997 266 ) FT was compared to individualtherapy in 80 adolescent and adult females with AN under outpatient treatment. FTproved to be more effective in younger patients at earlier stages of the disease than inadults with chronic disease.RCT1 +In an RCT (Eisler, 2000; UK) 267 conjoint FT (family treated as a whole) was comparedto FT in separate sessions for the parents and patients in 40 adolescent outpatients (98%females) with AN. Conjoint FT was more effective at reducing depression andobsessive behaviours, but not in weight restoration. In families where the mother’scritical attitude was significant separate FT was more effective.In an RCT (Geist, 2000; Canada) 268 FT was compared to group family psychoeducationin 25 adolescent females inpatients with AN. There were no differences in both groupsat 16 weeks.RCT1 ++RCT1 +In an RCT (Robin, 1994 269 ; USA and 1995 270 ) behavioural SFT (parents have controlover the patient’s renutrition) was compared to ego-oriented individual therapy in 24adolescent female inpatients and outpatients with AN. Behavioural SFT was moreeffective at increasing BMI and restoring menstruation. There were no differencesbetween both therapies in terms of diet and the behaviour of patients.RCT1 +In an RCT (Lock, 2005; USA) 271 long-term FT (20 sessions over 12 months) wascompared to short-term FT (10 sessions in 6 months) in adolescents (90% females)outpatients with AN. Long-term therapy presents better overall results in patients withdestructured families and improves BMI in patients with severe diet-related obsessions.RCT1 ++123CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Summary of the Evidence(See summary of the evidence for psychological treatment)CPG 30CPG 30CPG 30CPG 30CPG 30CPG 30SRSE 311++SRSE 311++SRSE 311++SRSE 311++SRSE 311++There is insufficient evidence to determine that conjoint or separate FT inchildren and adolescents is effective by the end of treatment and at posttreatmentfollow-up. (Eisler, 2000 267 ; Robin, 1999 272 ).There is limited evidence to determine that FT is superior to standard treatmentsin terms of achieving weight gain by the end of treatment and at post-treatmentfollow-up. (Crisp, 1991 263 ; Dare, 2001 264 ).In children and adolescents, there is insufficient evidence to determine that FTand body awareness therapy together are superior to FT alone (Wallin, 2000) 273 .There is limited evidence to determine that individual supportive psychotherapyis superior to FT in terms of weight gain in adults with AN at one year posttreatmentfollow-up (Russell, 1987) 265 .There is limited evidence to determine that FT is superior to supportivepsychotherapy at one-year follow-up in terms of weight gain and number ofrecoveries when administered to patients with AN (evolution under 3 years anddisorder onset age under 19 years) (Russell, 1987) 265 .There is insufficient evidence to determine group education in the family ismore effective than conjoint FT in terms of weight restoration in children andadolescents under inpatient treatment. (Geist, 2000) 268 .FT (including family of origin) can be more effective in young people with adisease of shorter duration.There are no studies that explore FT in adults including the insertion family(spouse and children) and not only the family of origin.There is no evidence to determine that FT helps adults with AN in chronicstages.Over time, different forms of FT produce good results in adolescents with AN.There is scarce evidence to determine that interventions involving the familyare more effective in patients under the age of 15 than in older patients.Recommendations(See also recommendations 9.GP.1. to 9.GP.11.)B 9.6.1.1.1. FT is indicated in children and adolescents with AN. (Adopted fromrecommendation 6.2.9.14. of the NICE guide).124CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

D 9.6.1.1.2. Family members of children with AN and siblings and family members ofadolescents with AN can be included in treatment, taking part inimproving communication, supporting behavioural treatment and sharingtherapeutic information. (Adopted from recommendation 6.2.9.13. of theNICE guide).D 9.6.1.1.3. Children and adolescents with AN can be offered individual appointmentswith health care professionals, separate from those in which the family isinvolved. (Adopted from recommendation 6.2.9.15.of the NICE guide).D 9.6.1.1.4. The effects of AN on siblings and other family members justifies theirinvolvement in treatment. (Adopted from recommendation 6.2.9.16. of theNICE guide).9.6.1.2. What is the safety of FT (systemic) in patients with AN?The answer in based on the NICE CPG (2004) 30 and on later SRSE 31, 202 . The updated search hasnot yielded any new evidence on the safety of FT in AN. Studies are briefly described inquestion 9.6.1.1.Scientific EvidenceIn an RCT (Crisp, 1991) 263 , 19% of participants dropped out of treatment. Dropouts pergroups were: G1: 40%; G2: 10%; G3: 15%; G4: 0%. No adverse effects were reported.In another RCT (Dare, 2001) 264 , 36% of participants dropped out of treatment. Dropoutsper groups were: FSP: 43%; FT: 27%; cognitive analytical therapy: 41%; and standardtreatments: 32%). No adverse effects were reported.RCT1 +RCT1 +In two additional RCTs (Russell, 1987 265 ; Eisler, 1997 266 ), 35% of treated patientsdropped out of treatment (FT, 37% and individual therapy, 33%). No adverse effectswere reported.RCT1 +In a further RCT (Eisler, 2000) 267 , 19% of patients dropped out of treatment. Dropoutsper groups were: conjoint FT: 11% and separate FT: 10%. No adverse effects werereported.RCT1 ++In an RCT (Geist, 2000) 268 , there were no dropouts. No adverse effects were reportedeither.In an RCT (Robin, 1994 269 y 1995 270 ), 8% of participants dropped out of treatment inboth groups. No adverse effects were reported.RCT1 +RCT1 +125CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

In an RCT (Lock, 2005) 271 , 20% of participants dropped out of treatment. 24% droppedout of long-term therapy and 18% dropped out of short-term therapy. Treatmentdropout as a result of another psychological treatment was reported as an adverseeffect.RCT1 ++Summary of the Evidence(See summary of the evidence for psychological treatment)CPG 30CPG 30In children and adolescents with AN there is insufficient evidence to determinethat separate or conjoint FT has more or less acceptability. (2 RCTs: N=64;Eisler, 2000 267 ; Robin, 1999 272 ).In children and adolescents with AN there is insufficient evidence to determinethat adding body awareness therapy to FT increases acceptability for patientsmore than FT alone (1 RCT; N=33;Wallin, 2000) 273 .Recommendations(See recommendations 9.GP.1. to 9.GP.11.)9.6.2. Bulimia nervosa9.6.2.1. What is the efficacy of FT (systemic) in patients with BN?There is no evidence to respond to this question in the NICE CPG (2004) 30 or in later SRSE 31, 211 .The updated search has identified two more RCTs.Scientific EvidenceIn a recent RCT (Schmith, 2007; UK)238 FT was compared (N=31 BN, N=10EDNOS) with CBT-GSH (N=30 BN, N=14 EDNOS) in adolescents between the agesof 13 and 20 years, with BN or EDNOS. Treatment was administered over 6 monthswith 12-month follow-up. CBT-GSH was more effective at reducing binge-eating at 6months than FT (p=0.03) even though this difference disappeared at 12 months. Therewere no differences between groups in terms of BMI, diet, eating fast and otherattitudinal eating disorder symptoms. The direct cost of treatment was lower for CBT-GSH and no differences were observed in other types of costs. CBT-GSH is slightlysuperior to FT in reducing binge-eating more quickly, being less costly and presentingbetter acceptability for adolescents with BN and/or EDNOS.In a recent RCT (Le Grange, et al., 2007; USA)274 FT (N=41) was compared to FSP(N=31). Patients receiving FT obtained significantly better results after treatment interms of binge-eating and purging abstinence (p=0.049). At 6-months follow-up bingeeatingand purging abstinence was statistically significant in favour of FT (12 patients,29%) compared to SFT (4 patients, 10%; p=0.005). In the measurement of all otherRCT1 ++RCT1++126CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

esults related with eating disorders a significant difference in favour of FT (p=0.003 top=0.03) was also reported. FT had a statistically significant clinical advantage overFSP after treatment and at 6-months follow-up. There was a reduction of BNsymptoms in the group treated with FT.9.6.2.2. What is the safety of FT (systemic) in patients with BN?Safety of FT is not addressed in the NICE CPG (2004) 30 or in later high-quality SRSE(1++) 31, 211 . Only one RCT has been identified that provides results on this issue. Studies arebriefly described in question 9.6.2.1.Scientific EvidenceIn an RCT (Schmith, 2007) 238 , 28% of young people refused to participate in the studydue to the family’s mandatory involvement, which suggests these patients should beoffered individual therapy.RCT1++Summary of the Evidence(See summary of the evidence for psychological treatment)Recommendations(See recommendations 9.GP.12. to 9.GP.17.)9.6.3. Binge-eating disorder9.6.3.1. What is the efficacy of FT (systemic or unspecified) in patients withBED?There is no evidence in the NICE CPG (2004) 30 , or in later high-quality SRSE 31, 245 . Theupdated search has identified one new RCT.Scientific EvidenceIn an RCT conducted by Schmith, 2007 238 that compared FT (N=31 BN; N=10 EDNOS)and CBT-GSH (N=30 BN; N=14 EDNOS) in adolescents aged 13-20 years with BN orEDNOS over 6 months with a 12-month follow-up, CBT-GSH was more effective atreducing binge-eating at 6 months than FT (p=0.03) even though this differencedisappeared at 12 months. There were no differences between groups in terms of BMI,diet, eating fast and other attitudinal eating disorder symptoms. The direct cost oftreatment was lower for CBT-GSH and no differences were reported in other types ofcosts.RCT1++127CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Summary of the Evidence(See summary of the evidence for psychological treatment)Recommendations(See recommendations 9.GP.12. to 9.GP.17.)9.6.3.2. What is the safety of FT (systemic or unspecified)in patients with BED?There is no evidence in the NICE CPG 30 or in later high-quality SRSE 31, 245 that address thesafety of FT. The updated search has identified one RCT. Studies are briefly described inquestion 9.6.3.1.In the RCT conducted by Schmith, 2007 238 28% of young people refused to participatein the study due to the family’s mandatory involvement, which suggests these patientsshould be offered individual therapy.RCT1++Summary of the Evidence(See summary of the evidence for psychological treatment)Recommendations(See recommendations 9.GP.12. to 9.GP.17.)9.7. Psychodynamic Therapy (PDT)9.7.1. Anorexia nervosa9.7.1.1. What is the efficacy and safety of PDT in patients with AN?There is no evidence that supports or denies the efficacy and safety of PDT in patients with AN.Recommendation(See also recommendations 9.GP.1. to 9.GP.11.)CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS128

9.7.2. Bulimia nervosa9.7.2.1. What is the efficacy of PDT in patients with BN?The answer to this question is based on the NICE CPG (2004) 30 , where it is described in terms ofseveral outcome variables. No evidence has been identified in later SRSE 31, 211 . The updatedsearch has not identified any new evidence on PDT in BN.Variables: reduction / remission of binge-eating andpurgingThere is insufficient evidence to determine that there are significant differencesbetween CBT and PDT in the frequency of binge-eating (1 RCT; N=46; Garner,1993 229 ; SMD: -0.19; 95% CI: -0.77 to 0.39) and purging (1 RCT; N=50; Garner,1993 229 ; SMD: -0.56; 95% CI: -1.13 to 0.01) by the end of treatment.RCT1++Variables: depression and/or interpersonal and psychosocial functioning and/orgeneral psychiatric symptomsThere is no evidence or insufficient evidence to determine that CBT-BN differs fromPDT in psychosocial and interpersonal functioning (1 RCT; N=41; Garner,1993 229 ;SMD: -0.39; 95% CI: -1.01 to 0.23) and in general psychiatric symptoms (1 RCT;N=48; Garner, 1993 229 ; SMD: -0.60; 95% CI: -1.18 to -0.02) by the end of treatment.RCT1++Summary of the Evidence(See also summary of the evidence for psychological treatment)CPG 30CBT does not offer any advantage over PDT.Recommendations(See recommendations 9.GP.12. to 9.GP.17.)9.7.2.2. What is the safety of PDT in patients with BN?The answer is based on the NICE CPG (2004) 30 , where different outcome variables aredescribed. No evidence has been identified in later SRSE 31, 211 . The updated search has notyielded any new evidence on PDT in BN.Scientific EvidenceThere is no significant evidence on the number of dropouts between CBT and PDT bythe end of treatment (1 RCT; N=50; Garner, 1993 229 ; RR: 1.00; 95% CI: 0.33 to 3.03).RCT1++129CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Summary of the Evidence(See summary of the evidence for psychological treatment)Recommendations(See recommendations 9.GP.12. to 9.GP.13.)9.7.3. Binge-eating disorder9.7.3.1. What is the efficacy and safety of PDT in patients with BED?There is no evidence that supports or denies the efficacy and safety of PDT in patients withBED.Summary of the Evidence(See summary of the evidence for psychological treatment)Recommendation(See recommendations 9.GP.12. to 9.GP.17.)9.8. Behavioural Therapy (BT)9.8.1. Anorexia nervosa9.8.1.1. What is the efficacy of BT in patients with AN?The answer is based on the NICE CPG 30 , where different outcome variables are described, on thehigh-quality SRSE (1++) elaborated by the AHRQ of the US (2006) 31 and on a more recentlypublished one (Bulik, et al., 2007) 202 . The updated search has not identified any new evidence onBT in AN.Scientific EvidenceAn RCT (Channon, 1989; UK) 215 compared CBT (N=8) to BT (N=8) and to FSP used ascontrol treatment (N=8) in women with AN (mean age for CBT: 21.6 years; BT: 24.1;control: 25.8) that underwent outpatient treatment over 12 months with 6-month followup.At 6 months of treatment, CBT was more effective than BT in improvingpsychosexual functioning; however, BT was more effective than CBT in improving theRCT1+130CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

menstrual cycle. At one year of treatment, BT was more effective at patient weightrestoration.Summary of the Evidence(See also summary of the evidence for psychological treatment)SRSE 311++CBT did not prove to be more effective than BT and FSP in terms of patientweight restoration, general behaviour and attitude regarding food.Recommendations(See recommendations 9.GP.1. to 9.GP.11.)9.8.1.2. What is the safety of BT in patients with AN?The answer is based on high-quality SRSE 31, 202 (1++). The updated search has not yielded anynew evidence on the safety of BT in AN. The study is briefly described in question 9.8.1.1.Scientific EvidenceAn RCT (Channon, 1989) 215 determined that 13% of patients dropped out of treatment.No adverse effects were reported.RCT1+Summary of the Evidence(See also summary of the evidence for psychological treatment)SRSE 311++Behavioural psychological interventions do not usually have any harmfuleffects on patients.Recommendations(See recommendations 9.GP.1 to 9.GP.11)9.8.2. Bulimia nervosa9.8.2.1. What is the efficacy of BT in patients with BN?The answer is based on the NICE CPG (2004) 30 , on the high-quality SRSE (1++)131CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

elaborated by the AHRQ of the US (2006) 31 and on a more recently published one (Shapiro, etal., 2007) 211 . The updated search has not identified any new evidence on the safety of BT in BN.Variables: reduction / remission of binge-eating and purgingIt is not likely that CBT-BN is more effective than BT in reducing the frequency ofbinge-eating (SMD: -0.11; 95% CI: -0.45 to 0.24) and purging (SMD: 0.08; 95% CI: -0.27 to 0.42) by the end of treatment, according to 3 RCTs (N=131; Fairburn, 1991 224 ;Freeman, 1988 220 ; Wolf, 1992 221 ).RCT1++Variables: depression and/or interpersonal and psychosocial functioningand/or general psychiatric symptomsThere is insufficient evidence to determine that CBT-BN differs from BT in terms ofgeneral psychiatric symptoms (1 RCT; N=33; Fairburn, 1991 224 ; SMD: -0.09; 95% CI:-0.79 to 0.61) and interpersonal and psychosocial functioning (1 RCT; N=32; Fairburn,1991 224 ; SMD: 0.14; 95% CI: -0.56 to 0.85) at follow-up.There is insufficient evidence to determine that CBT-BN differs from BT in thereduction of general psychiatric symptoms (SMD: -0.26; 95% CI: -0.89 to 0.37) and ininterpersonal and psychosocial functioning (SMD: -0.21; 95% CI: -0.84 to 0.42) by theend of treatment according to 1 RCT (N=39; Fairburn, 1991) 224 .There is insufficient evidence to determine that there are significant differences betweenBT and IPT in general psychiatric symptoms scores by the end of treatment (1 RCT;N=39; Fairburn, 1991 224 ; SMD: 0.09; 95% CI: -0.54 to 0.7) and at follow-up (1 RCT;N=31; Fairburn, 1991 224 ; SMD: 0.07; 95% CI: -0.65 to 0.78).There is insufficient evidence to determine that there are significant differences betweenBT and IPT in interpersonal and psychosocial functioning by the end of treatment (1RCT: N=39; Fairburn, 1991 224 ; SMD: -0.06; 95% CI: -0.69 to 0.55) and at follow-up (1RCT; N=31; Fairburn, 1991 224 ; SMD: -0.19; 95% CI: -0.91 to 0.52).In two RCTs (Fairburn, 1991; UK 224 and 1993 275 ) in 75 adult women with BN underoutpatient treatment, CBT was compared with BT and IPT. CBT was superior to BT at18 months of treatment in reducing symptoms related with diet, psychopathology andbody figure. CBT was more effective than IPT in reduction of vomiting. At 12-monthsfollow-up, CBT was superior to BT in abstinence of symptoms.RCT1++RCT1++RCT1++RCT1++RCT1+Summary of the Evidence(See also summary of the evidence for psychological treatment)SRSE 311++CBT is more effective than BT alone due to the cognitive component itincorporates, which seems to be the most important aspect. (Fairburn, 1991 224and 1993 275 ).132CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Recommendations(See recommendations 9.GP.12. to 9.GP.17.)9.8.2.2. What is the safety of BT in patients with BN?Information is based on An RCT included in high-quality SRSE 31, 211 . A brief description of thisRCT is presented in the section on efficacy. No new RCTs on the safety of BT in BN have beenidentified.Scientific EvidenceIn 2 RCTs (Fairburn, 1991 224 and 1993 275 ), 20% of treated patients dropped out oftreatment. In the BT group one case of severe weight loss was reported.RCT1+Summary of the Evidence(See summary of the evidence for psychological treatment)Recommendations(See recommendations 9.GP.12. to 9.GP.17.)9.8.3. Binge-eating disorder9.8.3.1. What is the efficacy and safety of BT in patients with BED?There is no evidence to support or deny the efficacy and safety of BT in patients with BED.Summary of the Evidence(See also summary of the evidence for psychological treatment)Recommendations(See recommendations 9.GP.12. to 9.GP.17.)133CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

SUMMARY OF THE EVIDENCE FORPSYCHOLOGICAL THERAPY(QUESTIONS 9.3. to 9.8.)Anorexia nervosaCPG 30CPG 30CPG 30CPG 30CPG 30SRSE 311++There is insufficient evidence to determine that a certain psychologicaltreatment (including CBT, IPT, SFT and BT) is more effective than anotherpsychological treatment for adults with AN by the end of treatment and at posttreatmentfollow-up. (6 RCTs; N=297; Bachar, 1999 276 ; Channon, 1989 215 ;Crisp, 1991 263 ; Dare, 2001 264 ; McIntosh, 2005 216 ; Treasure, 1995 277 ).There is limited evidence to determine that the outcomes of a certainpsychological treatment (including CBT, IPT, SFT, PDT and BT) are moreeffective at increasing body weight and that patients with AN should bereferred to reference centres (tertiary) by the end of treatment and at posttreatmentfollow-up (more than 5 years) (5 RCTs; N=258; Channon, 1989 215 ;Crisp, 1991 263 ; Dare, 2001 264 ; Hall, 1987 278 ; Treasure, 1995 277 ).There is insufficient evidence to determine that psychological treatment(including CBT, IPT, SFT, PDT and BT) has more or less acceptability forpatients with AN when compared to standard treatments (3 RCTs; N=198;Channon, 1989 215 ; Crisp, 1991 263 ; Dare, 2001 264 ).There is insufficient evidence to determine that psychological treatment(including CBT, IPT, SFT, PDT and BT) has more or less acceptability inadults with AN (6 RCTs; N=297; Bachar, 1999 276 ; Channon, 1989 215 ; Crisp,1991 263 ; Dare, 2001 264 ; McIntosh, 2005 216 ; Treasure, 1995 277 ).There is insufficient evidence to determine that psychological treatments (CBT,SFT and PDT) on an outpatient basis for patients with AN have more or lessacceptability in comparison with standard treatments (3 RCTs; N=198;Channon, 1989 215 ; Crisp, 1991 263 ; Dare, 2001 264 ).Current evidence on the efficacy of psychological treatment for AN is weak,with the exception of evidence relating to psychological treatment foradolescents with AN, which is moderate.Bulimia nervosaSRSE 311++In BN, evidence is strong for behavioural interventions and poor for SH (guidedor not).134CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

SRSE 311++The best psychological treatment of choice when individual and group CBT arenot effective in patients with BN remains unknown.Binge-eating disorderSRSE 311++In BED, evidence is moderate for behavioural interventions and weak for SH(guided or not).GENERAL RECOMMENDATIONS FORPSYCHOLOGICAL THERAPY IN EATINGDISORDERS(QUESTIONS 9.3. to 9.8.)Anorexia nervosaD 9.GP.1. The psychological therapies to be assessed for AN are: CBT, SFT, IPT,PDT and BT. (Adapted from recommendation 6.2.9.1. of the NICE guide).D 9.GP.2. In the case of patients who require special care, the selection of thepsychological treatment model that will be offered is even more important.(Adopted from recommendation 6.2.9.2. of the NICE guide).D 9.GP.3. The objective of psychological treatment is to reduce risk, to encourageweight gain by means of a healthy diet, to reduce other symptoms relatedwith eating disorders and to facilitate physical and psychological recovery(Adopted from recommendation 6.2.9.3. of the NICE guide).D 9.GP.4. Most psychological treatments for patients with AN can be performed onan outpatient basis (with physical monitoring) by professionals specialisedin eating disorders. (Adopted from recommendation 6.2.9.4. of the NICEguide).D 9.GP.5. The duration of psychological treatment should be of at least 6 monthswhen performed on an outpatient basis (with physical monitoring) and 12months for inpatients (Adopted from recommendation 6.2.9.5. of theNICE guide).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS135

D 9.GP.6. For patients with AN who have undergone outpatient psychologicaltherapy but have not improved or have deteriorated, the indication ofmore intensive treatments (combined individual and family therapy, day orinpatient care) must be considered. (Adopted from recommendation6.2.9.6. of the NICE guide).D 9.GP.7. For inpatients with AN, a treatment programme aimed at suppressingsymptoms and achieving normal weight should be established. Adequatephysical monitoring is important during renutrition. (Recommendation6.2.9.8. of the NICE guide is adopted).D 9.GP.8. Psychological treatments must be aimed at modifying behaviouralattitudes, attitudes related to weight and body shape and the fear of gainingweight. (Adopted from recommendation 6.2.9.9. of the NICE guide).D 9.GP.9. The use of excessively rigid behaviour modification programmes is notrecommended for inpatients with AN. (Adopted from recommendation6.2.9.10. of the NICE guide).D 9.GP.10. Following hospital discharge, patients with AN should be offeredoutpatient care that includes monitoring of normal weight restoration andpsychological intervention that focuses on eating behaviour, attitudes toweight and shape and the fear of social response regarding weight gain,along with regular physical and psychological follow-up. Follow-upduration must be of at least 12 months. (Recommendations 6.2.9.11. and6.2.9.12. of the NICE guide are adopted).D 9.GP.11. In children and adolescents with AN who require inpatient treatment andurgent weight restoration, age-related educational and social needs shouldbe taken into account. (Recommendation 6.2.9.17. of the NICE guide isadopted).Binge-Eating DisorderA 9.GP.12. Patients must be informed that all psychological treatments have a limitedeffect on body weight. (Adopted from recommendation 8.2.7.6. of theNICE guide).B 9.GP.13. A possible first step in the treatment of patients with BED is to encouragethem to follow a SH programme (guided or not). (Adapted fromrecommendation 8.2.7.2. of the NICE guide).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS136

B 9.GP.14. Health care professionals can consider providing BED patients with SHprogrammes (guided or not) that may yield positive results. However, thistreatment is only effective in a limited number of patients with BED.(Adapted from recommendation 8.2.7.3. of the NICE guide).D 9.GP.15. If there is a lack of evidence to guide the care of patients with EDNOS orBED, health care professionals are recommended to follow the eatingdisorder treatment that most resembles the eating disorder the patientpresents. (Adopted from recommendation 8.2.7.1. of the NICE guide).D 9.GP.16. When psychological treatments are performed on patients with BED, itmay be necessary in some cases to treat comorbid obesity. (Adopted fromrecommendation 8.2.7.7. of the NICE guide).D 9.GP.17. Adolescents with BED must be provided with psychological treatmentsadapted to their developmental stage. (Adopted from recommendation8.2.7.8. of the NICE guide).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS137

PHARMACOLOGICAL TREATMENTIn this section, scientific evidence on the efficacy and safety of several drugs studied for thetreatment of eating disorder patients is described. Only randomised controlled trials (RCT) ofsufficient quality have been included. The drugs assessed are included within the followinggroups: antidepressants, antipsychotics, appetite stimulants, opioid antagonists, anticonvulsants,psychostimulants and antiemetics.Although benzodiazepines such as alprazolam and lorazepam are indicated as anti-anxietydrugs no RCTs that address their use for eating disorders have been identified. A similarsituation has been encountered with lithium.9.9. AntidepressantsEvidence relating to eating disorders has been identified for the following antidepressants,according to the group they belong to:– Selective serotonin reuptake inhibitors (SSRIs): fluoxetine, citalopram, fluvoxamine.– Other antidepressants: sibutramine and trazodone.– Tricyclic antidepressants: amitriptyline, clomipramine and imipramine.9.9.1. Anorexia nervosa9.9.1.1. What is the efficacy of antidepressants in patients with AN?The answer is based on the NICE CPG (2004) 30 where the RCT results are described, on thehigh-quality SRSE (1++) elaborated by the AHRQ of the US (2006) 31 and on a more recentlypublished one conducted by Bulik, et al. (2007) 202 . The update search has not yielded any newevidence.Scientific EvidenceThere is limited evidence to indicate that there are significant differences betweenfluoxetine and placebo in body weight restoration in inpatients treated over one year (1RCT; N=35; Kaye, 2001 279 ; RR: 0.45; 95% CI: 0.23 to 0.86)In an RCT (Attia, 1998; USA) 280 fluoxetine (60 mg/day) was compared to placebo in 31female inpatients with AN (age: 16-45 years). Both groups experienced decreasedclinical symptoms related with eating disorders, obsessive-compulsive disorders,depressive behaviours and pre-occupation with food and its rituals. In both groups anincrease in the percentage of BMI was reported. There were no significant differencesbetween fluoxetine and placebo in any of the results.RCT1++RCT1++138CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

In an RCT (Kaye, 2001; USA) 279 fluoxetine was compared to placebo in 39 adult femaleinpatients and outpatients with AN. Patients, before being discharged, received20mg/day of fluoxetine, which was adjusted to a maximum dose of 60mg/day at 52weeks. The group treated with fluoxetine presented significant increases in BMI anddecreases in depression, anxiety, obsessive-compulsive disorders and symptoms relatedwith eating disorders.In an RCT (Biederman, 1985; USA) 281 amitriptyline (175 mg/day) was compared toplacebo in 25 patients and outpatients (age: 11-17 years) with AN. There were nosignificant differences in symptoms related with eating disorders, behaviour or weightwhen compared to placebo.In an RCT (Halmi, 1986; USA) 282 amitriptyline (160 mg/day) was compared tocyproheptadine (appetite stimulant) (32 mg/day) and to placebo in 72 female inpatients(age: 13-36 years). In the group treated with cyproheptadine, daily calorie intake wassignificantly greater than in the placebo group. In the groups treated with amitriptylineand cyproheptadine, weight restoration increased in less days than the placebo group.Patients with nonbulimic AN obtained better results with cyproheptadine than withamitriptyline or placebo.RCT1+RCT1+RCT1+Summary of the EvidenceSRSE 311++CPG 30SRSE 311++SRSE 311++The literature that exists on pharmacological treatment of AN is scarce andinconclusive. Most RCTs are based on small samples and very few of themhave statistical value to support their conclusions. Many studies includepatients who are receiving other treatment, whether it is psychological orpharmacological. As far as cases studied, they include inpatients that laterreceive outpatient treatment, which prevents generalisation of results.There is evidence that indicates significant differences in weight increase by theend of multimode treatment with antidepressants when compared to placebo (4RCT; N=146;Attia, 1998 280 [fluoxetine]; Biederman, 1985 281 [amitriptyline];Halmi, 1986 282 [amitriptyline]; Lacey, 1980 283 [clomipramine]).There is insufficient evidence to determine that there are significant differencesbetween antidepressants (citalopram) and wait-list in weight gain by the end ofoutpatient treatment (1 RCT; N=26; Fassino, 2002) 284 .Tricyclic antidepressants can be associated with improvement of disorderssecondary to eating disorders. However, these results are no associated withweight increase.Recommendations(See recommendations 9.GPH.1. to 9.GPH.6.)139CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

9.9.1.2. What is the safety of antidepressants in patients with AN?The answer is based on the NICE guide (2004) 30 , which describes RCT results based on variablesof interest, the high-quality SRSE (1++) elaborated by the AHRQ of the US (2006) 31 and on amore recently published one conducted by Bulik, et al. (2007) 202 . The updated search has notidentified any new evidence. The studies are briefly described in question 9.9.1.1.Scientific EvidenceThere is insufficient evidence to determine that there are significant differences betweenantidepressants and placebo that lead AN patients to drop out of treatment for anyreason, by the end of treatment (2 RCTs; N=47;Attia, 1998 280 [fluoxetine]; Lacey, 1980 283[clomipramine]; RR: 1.26; 95% CI: 0.44 to 3.56).In an RCT (Attia, 1998) 280 , one case of insomnia and agitation and one of blurred visionwere reported in the fluoxetine group. 3% of participants dropped out of treatment (intotal).In another RCT (Kaye, 2001) 279 no adverse effects were reported. Dropouts: 47% in thefluoxetine group and 85% in the placebo group.In an RCT (Biederman, 1985) 281 , the amitriptyline group presented diaphoresis (2 cases),drowsiness (6 cases), dry mouth (4 cases), blurred vision (1 case), urinary retention (1case), hypotension (2 cases) and leukopenia (1 case). Dry mouth (2 cases), palpitations(1 case) and dizziness (2 cases) were reported in the placebo group. There were nodropouts.In an RCT (Halmi, 1986) 282 the amitriptyline group presented drowsiness, excitement,confusion, increased motor activity, tachycardia, dry mouth and constipation. Thecyproheptadine group did not yield conclusive results. In the placebo group: excitementincreased motor activity and drowsiness. Dropouts: 30% amitriptyline, 25%cyproheptadina and 20% placebo.RCT1++RCT1++RCT1++RCT1+RCT1+Summary of the EvidenceCPG 30CPG 30There is insufficient evidence to determine that there are significant differencesbetween antidepressants (citalopram) and placebo that cause AN patients todropout of outpatient treatment due to adverse effects by the end of treatment (1RCT; N=26; Fassino, 2002) 284 .The dropout of patients who receive pharmacological treatment is important,especially in RCTs performed on outpatient cases.140CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

SRSE 311++SRSE 311++Due to the small-sized samples of both RCTs (Kaye, 2001 279 and Attia, 1998 280 )that use fluoxetine, no conclusions can be drawn regarding whether harmfuleffects associated with treatment in low-weight individuals differ from theharmful effects in normal weight individuals or those with psychiatricdisorders.In an RCT (Kaye, 2001) 279 , no adverse effects were reported in the fluoxetinegroup. In another RCT (Attia, 1998) 280 , one case of insomnia and agitation andone case of blurred vision were reported in the fluoxetine group. In regard totricyclic antidepressants, another RCT (Halmi, 1986) 282 with amitriptylinereported sporadic cases of associated drowsiness, excitement, confusion,increased motor activity, tachycardia, dry mouth and constipation; however, theproportion of adverse effects was similar between the experimental group andthe control group (placebo).Recommendations(See recommendations 9.GPH.1 to 9.GPH.6)9.9.2. Bulimia nervosa9.9.2.1. What is the efficacy of antidepressants in patients with BN?The answer is based on the NICE CPG (2004) 30 , which describes the RCT results basedon variables of interest, on the SRSE of sufficient quality (1++) elaborated by the AHRQ of theUS (2006) 31 and on a more recently published one by Shapiro, et al. (2007) 211 . The updated searchhas not identified any new evidence.Variable: BMIThere is not sufficient evidence to indicate clinically significant differences between SSRIantidepressants (fluoxetine) and placebo in relation to body weight by the end of treatment (1RCT; N=46; Kanerva, 1994 285 ; SMD: -0.30; 95% CI: -0.88 to 0.28).Variables: reduction / remission of binge-eating and purgingThere is limited evidence to determine that antidepressant treatment (fluoxetine,desipramine, phenelzine [withdrawn from the Spanish market], trazodone, bupropion) issuperior to placebo in the remission of binge-eating and purging by the end of treatment(6 RCTs; N=697; McCann, 1990262; Walsh, 1991286; Goldstein, 1995287; Walsh,1987288; Horne, 1988289; Pope, 1989290; RR: 0.88; 95% CI: 0.83 to 0.94; NNT: 9;95% CI: 6 to 15).RCT1++141CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

There is strong evidence that antidepressant treatment (fluoxetine, desipramine,phenelzine [withdrawn from the Spanish market], trazodone, bupropion) is superior toplacebo in clinical improvement (defined as reducing binge-eating by at least 50%) (6RCTs; N=855; Mc Cann, 1990 262 ; Walsh, 1991 286 ; Goldstein, 1995 287 ; Walsh, 1987 288 ;Horne, 1988 289 ; Pope, 1989 290 ; RR: 0.68; 95% CI:0.60 to 0.78; NNT: 5; 95% CI: 4 to 8).There is insufficient evidence to determine if there is a clinically significant differencebetween antidepressants (fluoxetine, desipramine, phenelzine [withdrawn from theSpanish market], trazodone, bupropion) and placebo in reducing the frequency of bingeeating(6 RCTs; N=290; McCann, 1990 262 ; Walsh, 1991 286 ; Walsh, 1987 288 ; Pope, 1989 290 ;Mitchell, 2001 258 ; Carruba, 2001 291 ; random effects model SMD: -0.33; 95% CI: -1.13 to0.47) and purging by the end of treatment (3 RCTs; N=198; Walsh, 1991 286 ; Pope1989 290 ; Mitchell, 2001 258 ; SMD: -0.19; 95% CI: -0.66 to 0.28).There is limited evidence to determine that MAOI treatment (phenelzine, [withdrawnfrom the Spanish market]) is superior to placebo in the remission of binge-eating andpurging by the end of treatment (1 RCT; N=62; Walsh, 1987 288 ; RR: 0.77; 95% CI: 0.62to 0.95; NNT: 5; 95% CI: 3 to 17).There is insufficient evidence to determine if there is a clinically significant differencebetween SSRI antidepressants (fluoxetine) and placebo in reducing the frequency ofbinge-eating (SMD: -0.30; 95% CI: -0.91 to 0.31) and purging (SMD: -0.56; 95% CI: -1.17 to 0.06) by the end of treatment according to 1 RCT (N=43; Kanerva, 2001) 285 .There is insufficient evidence to determine if there is a clinically significant differencebetween tricyclic antidepressants (desipramine) and placebo in reducing the frequency ofpurging (1 RCT; N=78; Walsh, 1991 286 ; SMD: -0.34; 95% CI: -0.79 to 0.11) by the endof treatment.There is strong evidence to determine that SSRI antidepressant treatment (fluoxetine) issuperior to placebo in reducing binge-eating (3 RCTs; N= 706; Goldstein, 1995 287 ;Kanerva, 1994 285 , Fluoxetine Bulimia Nervosa Collaborative Study Group, 1992 292 ; RR:0.73; 95% CI: 0.62 to 0.84; NNT: 6; 95% CI: 5 to 12) and purging by at least 50% by theend of treatment (2 RCTs; N=656; Goldstein, 1995 287 , Fluoxetine Bulimia NervosaCollaborative Study Group, 1992 292 ; RR: 0.66; 95% CI: 0.57 to 0.76; NNT: 5; 95% CI: 4to 7).There is strong evidence to determine that tricyclic antidepressant treatment(imipramine) is superior to placebo in terms of clinical improvement (defined asreducing binge-eating by at least 50%) by the end of treatment (1 RCT; N=22; Pope,1983 293 ; RR: 0.30; 95% CI: 0.11 to 0.80; NNT: 2; 95% CI: 2 to 4).There is strong evidence to determine that tricyclic antidepressants (imipramine,desipramine) vs. placebo decrease the frequency of binge-eating by the end of treatment(3 RCTs; N=120; Pope, 1983 293 ; McCann, 1990 262 ; Walsh, 1991 286 ; SMD:-0.82; 95% CI: -1.20 to -0.45).RCT1++RCT1++RCT1++RCT1++RCT1++RCT1++RCT1++RCT1++142CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Variables: depression and/or interpersonal and psychosocial functioning and/orgeneral psychiatric symptomsThere is limited evidence to determine that antidepressant treatment (fluoxetine,desipramine, phenelzine [withdrawn from the Spanish market], trazodone, bupropion) vs.placebo is superior at improving depression scores by the end of treatment (6 RCTs;N=293; McCann, 1990 262 ; Walsh, 1991 286 , Goldstein, 1995 287 ; Walsh, 1987 288 ; Horne,1988 289 ; Pope, 1989 290 ; SMD: -0.28; 95% CI: -0.51 to -0.05).There is insufficient evidence to determine that there are clinically significant differencesbetween SSRI antidepressants (fluoxetine) and placebo in depression scores by the end oftreatment (1 RCT; N=46; Kanerva, 2001 285 ; SMD: -0.44; 95% CI: -1.03 to 0.14).There is limited evidence to determine that tricyclic antidepressant treatment(imipramine, desipramine) is superior to placebo at improving depression scores by theend of treatment (3 RCT; N=120; Pope, 1983 293 ; McCann, 1990 262 ; Walsh, 1991 286 ; SMD:-0.47; 95% CI: -0.83 to -0.10).RCT1++RCT1++RCT1++Other resultsIn an RCT (Beumont, 1997;Australia) 294 fluoxetine was compared with placebo in 72adult female outpatients with BN. The fluoxetine group obtained better results in thereduction of binge-eating and vomiting, weight restoration, pre-occupation with food,EDI’s BN scores, obsession regarding slimness and body dissatisfaction. There were nodifferences in depression scores.In an RCT (Fichter, 1991; Germany) 295 fluoxetine was compared with placebo in 39 adultfemale inpatients with BN. There were no differences in any of the outcomes measured.In an RCT (Romano, 2002; USA) 296 fluoxetine was compared with placebo in 150patients (98% women) with BN under outpatient treatment. The fluoxetine groupobtained better results than the placebo group in the reduction of vomiting, binge-eating,disordered behaviour, rituals, pre-occupation and other severe symptoms.In two RCTs (Fichter, 1996; Germany 297 ; Fichter, 1997 298 ) fluvoxamine was comparedwith placebo in 72 adult female outpatients with BN. The fluvoxamine group obtainedbetter results in the reduction of vomiting, purging and binge-eating frequencies whencompared with the placebo group. Both groups gained weight, with no significantdifferences between them.RCT1+RCT1++RCT1+RCT1++143CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Summary of the EvidenceSRSE 311++SRSE 311++SRSE 311++SRSE 311++SRSE 311++SRSE 311++The fluoxetine dose (60 mg/day) administered over 6 to 18 weeks has managed,in all moderate (1+) and high quality (1++) RCT, to reduce binge-eating andpurging as well as psychological symptoms related with eating disorders in ashort period of time.Fluoxetine at 60mg/day obtains better results than a 20mg/day dose (FluoxetineBulimia Nervosa Collaborative Study Group, 1992) 292 ; this dose is also associatedwith relapse prevention in a study with a considerable amount of discontinuation.There is considerable evidence of the short-term effect of fluoxetine treatment(60mg/day) in patients with BN. There is no evidence of the effectiveness oflong-term treatment or the optimal duration of treatment.Some studies have reported remissions in a small number of patients treatedexclusively with pharmacological treatment, which leads us to borne in mindthat although symptoms improve, they persist in time and do not disappear.In an RCT (Walsh, 1991) 286 it was reported that patients with greater body massand weight and longer disease length responded better to desipraminetreatment.In the study Fluoxetine Bulimia Nervosa Collaborative Study Group,1992 292 , patients with greater weight responded better in all treatment groups.Recommendations(See also recommendations 9.GPH.1. to 9.GPH.6.)B 9.9.2.1.1. Patients should be informed that antidepressant treatment can reduce thefrequency of binge-eating and purging episodes but effects are notimmediate. (Adopted from recommendation 7.3.6.2. of the NICE guide).B 9.9.2.1.2. In the treatment of BN pharmacological treatments other thanantidepressants are not recommended. (Adopted from recommendation7.3.6.4. of the NICE guide).D 9.9.2.1.3. The dose of fluoxetine used in patients with BN is greater than the doseused for treating depression (60 mg/day). (Adopted from recommendation7.7.6.5. of the NICE guide).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS144

D 9.9.2.1.4. Amongst SSRI antidepressants, fluoxetine is the first-choice drug fortreatment of BN, in terms of acceptability, tolerability and symptomreduction. (Adopted from recommendation 7.3.6.3. of the NICE guide).9.9.2.2. What is the safety of antidepressants in patients withBN?The answer is based on the NICE CPG (2004) 30 , which describes the results obtainedfrom RCTs, on the high-quality SRSE (1++) elaborated by the AHRQ of the US (2006) 31 and ona more recently published one by Shapiro, et al. (2007) 211 . The updated search has not identifiedany new evidence. The studies are briefly described in question 9.9.2.1.Scientific EvidenceThere is limited evidence to suggest that antidepressant treatment (fluoxetine,desipramine, imipramine, phenelzine [withdrawn from the Spanish market], trazodone,mianserine, moclobemide) is superior to placebo in treatment discontinuation due toadverse effects (9 RCTs; N=1.078; Pope, 1983 293 , 1989 290 ; Mitchell, 1990 243 ; Walsh,1991 286 ; 1987 288 ; Kanerva, 1994 285 ; Goldstein, 1995 287 ; Fluoxetine Bulimia NervosaCollaborative Study Group, 1992 292 ; Carruba, 2001 291 ; RR: 1.90; 95% CI: 1.20 to 2.99;NNH: 20; 95% CI: 13 to 50).There is insufficient evidence to suggest which types of antidepressants (fluoxetine,desipramine, imipramine, phenelzine [withdrawn from the Spanish market], trazodone,mianserine, moclobemide, brupopion) are well or poorly tolerated by patients with BN(13 RCTs; Pope, 1983 293 , 1989 290 ; Mitchell, 1990 243 , 2001 258 ; Walsh, 1991 286 , 1987 288 ,2004 225 ; Kanerva, 1994 285 ; Goldstein, 1995 287 ; Fluoxetine Bulimia Nervosa CollaborativeStudy Group, 1992 292 ; Carruba, 2001 292 ; McCann, 1990 262 ; Sabine, 1983 299 ; Horne, 1988 289 ;N=1.336; random effects model RR: 0.91; 95% CI:0.72 to 1.16).RCT1++RCT1++There is limited evidence suggesting that treatment with antidepressants (fluoxetine,desipramine) vs. placebo favours treatment acceptability (5 RCTs Mitchell, 2001 258 ;Walsh, 1991 286 , 2004 233 ; Kanerva, 1994 285 ; Goldstein, 1995 287 , Fluoxetine BulimiaNervosa Collaborative Study Group, 1992 292 ; N=803; RR:0.79; 95% CI: 0.67 to 0.95).There is insufficient evidence suggesting that there are significant differences betweenSSRI antidepressants (fluoxetine) and placebo in the number of patients who discontinuetreatment due to adverse effects (3 RCTs Kanerva, 1994 285 ; Goldstein, 1995 287 ,Fluoxetine Bulimia Nervosa Collaborative Study Group, 1992 292 ; N=706; RR: 1.59; 95%CI: 0.88 to 2.88).There is strong evidence to determine that the dropout rate is greater in the placebogroup than in the group receiving tricyclic antidepressants (imipramine, desipramine) (4RCTs; N=217; Pope, 1983 293 , Mitchell, 1990 243 ; Walsh, 1991 286 ; McCann, 1990 262 ; RR:2.03; 95% CI: 1.18 to 3.49; NNT: 7; 95% CI: 4 to 20).RCT1++RCT1++RCT1++145CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

There is insufficient evidence suggesting that there are significant differences betweentricyclic antidepressants (imipramine, desipramine) and placebo in the number ofpatients who discontinue treatment due to adverse effects (3 RCTs; N=187; Pope,1983 293 ; Mitchell, 1990 243 ; Walsh, 1991 286 ; RR: 3.17; 95% CI: 0.84 to 11.90).There is insufficient evidence to determine that there is a significant difference betweenMAOI antidepressants (phenelzide [withdrawn from the Spanish market] andmoclobemide) and placebo in the number of patients who discontinue treatment due toadverse effects (random effects model RR: 2.55; 95% CI: 0.20 to 33.22) or any otherreason (random effects model RR: 0.94; 95% CI: 0.50 to 1.77; based on 2 RCTs;N=139; Walsh, 1987 288 ; Carruba, 2001 291 ).In an RCT (Beumont, 1997) 294 fluoxetine was compared with placebo. Adverse effects inthe fluoxetine group included: insomnia, nausea and instability, the latter beingsignificantly more common. Depression was the most common adverse effect in theplacebo group. No dropouts were reported.In an RCT (Fichter, 1991) 295 , that compared fluoxetine vs. placebo, the experimentalgroup showed greater tremor (significant differences). No dropouts were reported.In an RCT (Romano, 2002) 296 fluoxetine was compared with placebo. This studyexplored the efficacy of fluoxetine (60mg/day) in the number of relapses over 52 weeks.Relapses were less frequent in the placebo group (33% vs. 51% in the fluoxetine group).Treatment discontinuation occurred more frequently within the first 3 months of the 52weeks of complete treatment. The same study reported a dropout rate of 83% in thefluoxetine group and 92% in the placebo group. Rhinitis was reported to be the adverseeffect. (fluoxetine, 24 cases; placebo, 12 cases; p

9.9.3. Binge-Eating Disorder9.9.3.1. What is the efficacy of antidepressants in patients with BED?The answer is based on the NICE CPG 30 , which describes RCT results based on variables ofinterest, on the high-quality SRSE (1++) elaborated by the AHRQ of the US (2006) 31 and on amore recently published one conducted by Brownley, et al. (2007) 245 . The updated search has notidentified any new evidence.Variable: BMIThere is evidence suggesting that there are no clinically significant differences betweenantidepressants (fluoxetine, imipramine, sertraline) and placebo in terms of body weight(BMI when possible) by the end of treatment (3 RCTs; N=95; Arnold,2002 301 ; McElroy,2000 302 ; Laederach, 1999 303 ; SMD: 0.00; 95% CI: -0.42 to 0.42).RCT1++Variable: reduction / remission of binge-eating and purgingThere is limited evidence to determine that there are clinically significant differencesbetween antidepressants (fluoxetine, fluvoxamine, sertraline, imipramine and citalopram)and placebo in favour of antidepressants in terms of binge-eating remission (4 RCTs;N=217; Arnold, 2002 301 ; McElroy, 2000 302 ; 2003 304 ; Hudson, 1998 305 ; RR: 0.75; 95% CI:0.62 to 0.90; NNT: 5; 95% CI: 4 to 13) and reduction of binge-eating frequency by theend of treatment (4 RCTs; N=122; Arnold, 2002 301 ; McElroy, 2000 302 , 2003 304 ; Laederach,1999 303 ; SMD: -0.59; 95% CI: -0.96 to -0.22).There is limited evidence to suggest that there are clinically significant differencesbetween tricyclic antidepressants (imipramine) and placebo in favour of tricyclicantidepressants in terms of reducing the frequency of binge-eating by the end oftreatment (1 RCT; N=29; Laederach, 1999 303 ; SMD: -0.77; 95% CI: -1.53 to -0.01).RCT1++RCT1++Variable: depressionThere is insufficient evidence to determine that tricyclic antidepressants (imipramine) aresuperior to placebo in terms of reducing depression scores (1 RCT; N=29; Laederach,1999 303 ; SMD: -0.73; 95% CI: -1.49 to 0.02).RCT1++Other resultsAn RCT (Pearlstein, 2003; USA) 306 compared fluvoxamine (average dose 239 mg/day) vs.placebo over 12 weeks in 20 adult outpatients (88% women) with BED. There were nodifferences between both groups in terms of frequency of binge-eating, but both groupsshowed a decrease in frequency of binge-eating, loss of body weight and size andreduced self-reported depression.RCT1++147CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

An RCT (Appolinario, 2003; Brazil) 307 compared sibutramine vs. placebo in outpatientswith BED (88% women; mean age 35.2 to 36.6). Sibutramine is associated withdecreased depressive behaviour and is superior to placebo in reducing the frequency andseverity of binge-eating episodes. In the placebo group weight gain was observed duringand by the end of treatment. In the group treated with the drug, weight loss by the end oftreatment was reported.RCT1++Summary of the EvidenceSRSE 311++SRSE 311++In short-term RCTs with SSRI antidepressants, the group treated with thesedrugs presents better results in the reduction of symptoms related with eatingdisorders, in behaviour, weight and severity of the disease. The clinical impactof these conclusions cannot be judged due to the lack of data on total BEDremission and on follow-up.Low doses of imipramine as a complementary strategy to nutritionalcounselling and psychological therapy are associated with reduced binge-eatingand weight loss that is sustained after drug discontinuation.Recommendations(See also recommendation 9.GPH.6.)B 9.9.3.1.1. SSRI antidepressant treatment can be offered to a patient with BED,regardless of whether he/she follows a guided SH programme or not.(Adopted from recommendation 8.3.5.1. of the NICE guide).B 9.9.3.1.2. Patients must be informed that SSRI antidepressant treatment can reducethe frequency of binge-eating, but the duration of long-term effects isunknown. Antidepressant treatment may be beneficial for a small numberof patients. (Adopted from recommendation 8.3.5.2. of the NICE guide).9.9.3.2. What is the safety of antidepressants in patients with BED?The answer is based on the NICE CPG (2004) 30 , which describes the results of RCTs, onthe high-quality SRSE (1++) elaborated by the AHRQ of the US (2006) 31 and a more recentlypublished one carried out by Brownley, et al. (2007) 245 . The updated search has not identifiedany new evidence. Studies are briefly described in question 9.9.3.1.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS148

Scientific EvidenceThere is insufficient evidence to determine if there is a clinically significant differencebetween antidepressants (fluoxetine, fluvoxamine, sertraline, imipramine andcitalopram) and placebo in treatment discontinuation for any reason (5 RCTs; N=248;Arnold, 2002 301 ; McElroy, 2000 302 , 2003 304 ; Hudson, 1998 305 ; Laederach, 1999 303 ; randomeffects model RR: 1.02; 95% CI: 0.43 to 2.42).RCT1++There is insufficient evidence to determine if there is a clinically significant differencebetween antidepressants (fluoxetine, fluvoxamine, sertraline) vs. placebo in treatmentdiscontinuation due to adverse effects (3 RCTs; N=176; Arnold, 2002 301 ; McElroy,2000 302 ; Hudson, 1998 305 ; RR: 2.48; 95% CI: 0.74 to 8.39).RCT1++There is insufficient evidence to determine if there is a clinically significant differencebetween antidepressants (fluoxetine, fluvoxamine, sertraline and citalopram) andplacebo in treatment discontinuation for any reason (4 RCTs; N=217; Arnold, 2002 301 ;McElroy, 2000 302 , 2003 304 ; Hudson, 1998 305 ; random effects model RR: 1.02; 95% CI:0.39 to 2.68) or as a result of adverse effects by the end of treatment (3 RCTs; N=183;Arnold, 2002 301 ; McElroy, 2003 304 ; Hudson, 1998 305 ; RR: 3.03; 95% CI: 0.84 to 10.86).There is insufficient evidence to determine if there is a clinically significant differencebetween tricyclic antidepressants (imipramine) and placebo in treatment discontinuationdue to adverse effects or any other reason (1 RCT; N=31; Laederach, 1999 303 ; RR: 1.07;95% CI: 0.07 to 15.57).In an RCT (Pearlstein, 2003) 306 that compared fluovoxamine with placebo, 20% ofparticipants dropped out of treatment.In an RCT (Appolinario, 2003) 307 , 23% of participants in the sibutramine group and 17%of participants in the placebo group dropped out of treatment. The adverse effects ofsibutramine were: dry mouth (22 cases); headache (6); constipation (7). In the placebogroup: dry mouth (3); headache (14); constipation (0) (p

9.10. AntipsychoticsEvidence in AN has been identified for the following Antipsychotics:sulpiride, pimozide and olanzapine.9.10.1. Anorexia nervosa9.10.1.1. What is the efficacy of Antipsychotics in patients with AN?The answer is based on the NICE CPG (2004) 30 and on a high-quality SRSE (1++)(Dunican,2007) 308 . The updated search has not yielded any new evidence.Scientific EvidenceThere is insufficient evidence to determine that ant psychotics (pimozide and sulpiride)have an impact on body weight vs. placebo during multimode treatment of inpatientswith AN (2 crossed studies; N=32; pimozide [Vandereycken, 1982] 309 and sulpiride[Vandereycken, 1984] 310 ).There is insufficient evidence to determine that there is any significant differencebetween antipsychotics and antidepressants in terms of weight gain in cases of AN.RCT1++RCT1++Summary of the EvidenceSRSE 3081++SRSE 3081++In some of the case series and in most of the RCTs, patients with AN gainedweight while receiving treatment with olanzapine, achieving healthy weight inmany cases. Reported cases and RCTs identified additional benefits ofolanzapine, including the reduction of delusional beliefs, improvement of bodyself-image, decrease of agitation and anxiety prior to meals, improvement ofsleep, depressive symptoms and treatment adherence and other symptomsrelated with eating disorders.Preliminary evidence supports the use of olanzapine for the treatment of AN,demonstrating that a 2.5 to 15 daily mg dose promotes weight gain and haspositive effects on related psychological symptoms. The limitations of the dataanalysed are: small sample, high dropout rate in the RCT and the open designof the RCT.Summary of the Evidence(See also recommendations 9.GPH.1. to 9.GPH.6.)150CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

9.10.1.2. What is the safety of Antipsychotics in patients with AN?The answer is based on the NICE CPG (2004) 30 . The updated search has not yielded any newevidence.Scientific EvidenceThere is insufficient evidence, stemming from 2 small studies, to determine if there is aclinically significant difference between antipsychotics (pimozide and sulpiride) andplacebo in terms of dropout rate due to adverse effects or any other reason by the end oftreatment (2 crossed studies; N=32; pimozide [Vandereycken, 1982] 309 and sulpiride[Vandereycken, 1984] 310 ).RCT1++Recommendations(See recommendations 9.GF.1.to 9.GPH.6.)9.11. Appetite stimulants (orexigens)Of the group of appetite stimulants, evidence of cyproheptadine in AN has beenidentified. No evidence has been identified on the use of pizotifen (also an appetite stimulant) inAN.9.11.1. What is the efficacy of cyproheptadine in patients with AN?The answer is based on en la NICE CPG (2004) 30 . The updated search has not yielded anynew evidence.Scientific EvidenceThere is insufficient evidence to determine that Antipsychotics or antihistamines(cyproheptadine) have any impact on body weight when compared to placebo in patientswith AN who are under inpatient management and under multimode treatment whencompared to placebo (2 RCTs; N=177; Goldberg, 1980 311 ; Halmi, 1986 282 ).RCT1++Recommendations(See recommendations 9.GPH.1 to 9.GF.6)151CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

9.11.2. What is the safety of cyproheptadine in patients with AN?The answer is based on the NICE CPG (2004) 30 . The updated search has not yielded any newevidence.Scientific EvidenceThere is insufficient evidence to determine that antidepressants, antihistamines orantipsychotics are more or less acceptable to patients with AN when compared toplacebo or wait-list.There is insufficient evidence to determine that antidepressants, antihistamines orantipsychotics produce more or less adverse effects in patients with AN when comparedwith placebo or wait-list.RCT1++RCT1++Recommendations(See recommendations 9.GPH.1. to 9.GPH.6.)9.12. Opioid antagonistsEvidence has been found for the following opioid antagonist in the treatment of BN:naltrexone. No evidence on the use of naloxone (also an opioid antagonist) in BNT/BEDtreatment has been found.9.12.1. Bulimia nervosa9.12.1.1. What is the efficacy of naltrexone in patients with BN?The answer is based on the NICE CPG (2004) 30 . The updated search has not yielded anynew evidence.Scientific EvidenceThere is insufficient evidence to determine that opioid antagonists (naltrexone) aremore or less effective when compared to placebo in women with mean age 25 yearsdiagnosed with BN (2 RCT; N=28; Huseman, 1990 312 ; Mitchell, 1989 313 ).RCT1++Recommendations(See recommendations 9.GPH.1. to 9.GPH.6.)152CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

9.12.1.2. What is the safety of opioid antagonists in patients with BN?The answer is based on the NICE CPG (2004) 30 . The updated search has not yielded any newevidence.Scientific EvidenceThere is insufficient evidence to determine that opioid antagonists (naltrexone) are moreor less acceptable to patients when compared to placebo in women with mean age 25years who have been diagnosed with BN (2 RCTs; N=28; Huseman, 1990 312 ; Mitchell,1989 313 ).RCT1++Recommendations(See recommendations 9.GPH.1. to 9.GPH.6.)9.13. Topiramate9.13.1. Bulimia nervosa9.13.1.1. What is the efficacy of topiramate in patients with BN?Evidence is based on the high-quality SRSE (1++) elaborated by the AHRQ of the US(2006) 31 and also on a more recently published high-quality SRSE (1++) (Shapiro, et al., 2007) 211 .The updated search has not identified any new evidence.Scientific Evidence2 RCTs (Hoopes, 2003; USA 314 ; Hedges, 2003; USA 315 ) compared topiramate vs. placeboin 68 adult patients (97% women) with BN who were being treated on an outpatientbasis. The proportion of abstinence from binge-eating and purging was 22.6% in thetopiramate group and 6% in the placebo group, a non-significant difference. Thetopiramate group was associated with significant reduction of anxiety but not depression,and with a greater tendency towards weight loss. The control group had a tendencytowards weight gain.RCT1+Recommendations(See recommendations 9.GPH.1. to 9.GPH.6.)153CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

9.13.1.2. What is the safety of topiramate in patients with BN?Evidence is based on two RCTs included in the high-quality SRSE (1++) elaborated bythe AHRQ of the US (2006) 31 and also on a more recently published high-quality SRSE (1++)conducted by Shapiro, et al. (2007) 211 . The updated search has not identified any new evidence.The studies are briefly described in question 9.13.1.1.Scientific EvidenceIn the two previous RCTs (Hoopes, 2003 314 ; Hedges, 2003 315 ) one case of adverse effectwas reported in the form of facial rash and irritability in the topiramate group. Theoverall dropout rate was higher (47%) in the placebo group than in the topiramate group(34%).RCT1+Recommendations(See recommendations 9.GPH.1. to 9.GPH.6.)9.13.2. Binge-Eating Disorder9.13.2.1. What is the efficacy of topiramate in patients with BED?The answer is based on the NICE CPG (2004) 30 , on the high-quality SRSE (1++)elaborated by the AHRQ of the US (2006) 31 and on a more recently published high-quality SRSE(1++) conducted by Brownley, et al. (2007) 245 . The updated search has no identified any newevidence.Scientific EvidenceIn an RCT (McElroy, 2003; USA) 304 topiramate (average dose 212 mg/day) wascompared to placebo in 61 patients with eating disorders over 14 weeks on an outpatientbasis. Patients who received topiramate presented remission of binge-eating andsignificant reduction of its frequency. There were significant differences in weight lossbetween the group treated with topiramate (5.9 kg) and the placebo group (1.2 kg).There were no differences between groups in terms of depression scores 31 .There is limited evidence to suggest that there may be a clinically significant differencebetween topiramate and placebo in the remission of binge-eating by the end of treatment(1 RCT; N=61; McElroy, 2003 304 ; RR: 0.56; 95% CI: 0.34 to 0.92; NNT: 4; 95% CI: 2 to15).RCT1+RCT1++Recommendations(See recommendations 9.GPH.1. to 9.GPH.6.)154CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

9.13.2.2. What is the safety of topiramate in patients with BED?The answer is based on the NICE CPG 30 , where the results of RCTs are described basedon variables of interest, on the high-quality SRSE (1++) elaborated by the AHRQ of the US(2006) 31 and on a more recently published high-quality SRSE (1++) conducted by Brownley, etal. (2007) 245 . The updated search has no identified any new evidence. The studies are brieflydescribed in question 9.13.2.1.Scientific EvidenceThere is insufficient evidence to determine that there are clinically significantdifferences between topiramate (anticonvulsant) and placebo in the number of patientswho drop out of treatment for any reason (RR: 1.21; 95% CI: 0.67 to 2.16) or due toadverse effects (RR: 2.07; 95% CI: 0.57 to 7.52) based on 1 RCT (1 RCT; N=61;McEnroy, 2003) 304 .According to An RCT (McElroy, 2003) 304 , the following adverse effects were reported:headache, paresthesia and amenorrhoea in the topiramate group. In the placebo group:cramps, sedation and testicular pain. The overall dropout rate was 47% in the topiramategroup and 39% in the placebo group.RCT1++RCT1+Recommendations(See recommendations 9.GPH.1. to 9.GPH.6.)9.14. Atomoxetine9.14.1. What is the efficacy of atomoxetine in patients witheating disorders?No evidence has been found in the NICE CPG (2004) 30 or in the high-quality SRSE 31, 202, 211, 245 .The updated search has identified one RCT.Scientific EvidenceOne RCT (McElroy, 2007) 316 compared atomoxetine (40-120 mg/day doses; N=20) vs.control group (N=19) over 10 weeks in a group of patients with BED (age: 18 to 65years). The group treated with atomoxetine significantly reduced the weekly frequency ofbinge-eating (p=0.018), the daily frequency of binge-eating (p=0.003) and the diseasescale (p=0.015). No significant differences were found in other results. 30% of patientsin the treated group and 45% in the placebo group did not complete the study.RCT1+155CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Recommendations(See recommendations 9.GPH.1. to 9.GPH.6.)9.14.2. What is the safety of atomoxetine in patients witheating disorders?The answer is based on the RCT described in the question regarding efficacy.Scientific EvidenceAn RCT (McElroy, 2007) 316 compared atomoxetine (40 a 120 mg/day doses; N=20) vs.control group (N=19) over 10 weeks in a group of patients with BED (age: 18 to 65 years). Therewere 3 dropouts due to adverse effects in the treated group (depressive symptoms, constipationand agitation) and 1 in the placebo group. Atomoxetine is effective and well tolerated in the shorttermtreatment of BED. RCT 1+Recommendations(See recommendations 9.GPH.1. to 9.GPH.6.)9.15. Antiemetics9.15.1. Bulimia nervosa9.15.1.1. What is the efficacy of ondansetron in patients with BN?The answer is based on the NICE CPG (2004) 30 , on the high-quality SRSE (1++)elaborated by the AHRQ of the US (2006) 31 and on a more recently published high-quality SRSE(1++) conducted by Shapiro, et al. (2007) 211 . The updated search has no identified any newevidence.Scientific EvidenceAn RCT (Faris, 2000; USA) 317 compared ondansetron treatment to placebo in adultfemales with BN (N=26) who were being treated on an outpatient basis over 4 weeks.In the ondansetron group frequency of binge-eating and purging decreased significantlyand the restoration of a well-balanced diet improved. There are no measures ofdepression or anxiety. There are no differences in patients’ weight changes.RCT1++156CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Summary of the EvidenceCPG 30There is insufficient evidence to determine that antiemetics (ondansetron) aremore or less effective when compared to placebo (2 RCTs; N=37; Faris, 1998 317 ,2000 317 ).Recommendations(See recommendations 9.GPH.1. to 9.GPH.6.)9.15.1.2. What is the safety of ondansetron in patients with BN?The answer is based on the NICE CPG (2004) 30 , on the high-quality SRSE (1++)elaborated by the AHRQ of the US (2006) 31 and on a more recently published high-quality SRSE(1++) conducted by Shapiro, et al. (2007) 211 . The updated search has no identified any newevidence. The study is briefly described in question 9.15.1.1.Scientific EvidenceIn an RCT (Faris, 2000) 317 , one participant dropped out of treatment in the ondansetrongroup and there were no dropouts in the placebo group. No adverse effects werereported.RCT1++Summary of the EvidenceCPG 30There is insufficient evidence to determine that antiemetics (ondansetron) aremore or less acceptable vs. placebo (2 RCTs; N=37; Faris, 1998 317 , 2000 317 ).Recommendations(See recommendations 9.GPH.1. to 9.GPH.6.)157CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

SUMMARY OF THE EVIDENCE FORPHARMACOLOGICAL TREATMENT(QUESTIONS 9.9. to 9.15.)SRSE 311++Dropout rates in the RCT assessing pharmacological treatments ranged from0% to 51% of treated cases. No drug in particular showed a greater relapse ratethan others.Anorexia nervosaSRSE 311++The literature relating to medication in AN is scarce and inconclusive.Binge-Eating DisorderSRSE 311++There is moderate evidence that supports the role of drugs in the treatment of BED.GENERAL RECOMMENDATIONS FOR THEPHARMACOLOGICAL TREATMENT OF EATINGDISORDERS(QUESTIONS 9.9. to 9.15.)Anorexia nervosaD 9.GPH.1. Pharmacological treatment is not recommended as the only primarytreatment in patients with AN. (Adopted from recommendation 6.3.6.1. ofthe NICE guide).D 9.GPH.2. Caution should be exercised when prescribing pharmacological treatmentfor patients with AN who have associated comorbidities such as obsessivecompulsivedisorder (OCD) or depression. (Adopted fromrecommendation 6.3.6.2. of the NICE guide).D 9.GPH.3. Given the risk of heart complications presented by patients with AN,prescription of drugs whose side effects may affect cardiac function mustbe avoided. (Adopted from recommendation 6.3.6.4. of the NICE guide).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS158

D 9.GPH.4. If drugs with adverse cardiovascular effects are administered, ECGmonitoring of patients should be carried out. (Adopted fromrecommendation 6.3.6.3. of the NICE guide).D 9.GPH.5. All patients with AN must be warned of the side effects ofpharmacological treatments. (Adopted from recommendation 6.3.6.5. ofthe NICE guide).Binge-Eating DisorderD9.GPH.6In the absence of evidence to guide the management of BED, it isrecommended that the clinician treat the patient based on the eating problemthat most closely resembles the patient’s eating disorder according to BN orAN guides. (Adopted from recommendation 8.2.7.1. of the NICE guide).159CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

COMBINED INTERVENTIONSThis section describes the evidence for the efficacy and safety of combined interventions,whether they are psychological or pharmacological, in the treatment of eating disorders.Occasionally, the experimental and control groups receive one or more treatments.9.16. What is the efficacy and safety of combinedinterventions in patients with eating disorders?9.16.1. Anorexia nervosa9.16.1.1. What is the efficacy and safety of combined interventionsin patients with AN?The answer is based on the NICE CPG (2004) 30 , which describes the results from theRCT according to variables of interest. There are no results regarding combined interventionsneither in the quality systematic review of scientific evidence (1++) elaborated by the AHRQ ofthe US (2006) 31 nor in the more recent one conducted by Bulik, et al. (2007) 202 . The updatedsearch has identified two new 2 RCTs.The revised literature does not inform on the adverse effects declared over thecourse of the RCT that studied combined interventions on AN.Scientific evidenceIn patients whose clinical picture is not as severe as to require emergency treatment,there is insufficient evidence on whether to administer an outpatient psychologicaltreatment or to proceed to a complete hospitalisation for administration of suchtreatment (group therapy-FT-NC vs. individual therapy-NSFT-NC) according to 1RCT (N=90; Crisp, 1991) 263 .An RCT (Brambilla, 2007, Italy) 318 comprised of 30 women with AN receivingoutpatient treatment compared CBT-olanzapine (daily doses 2.5 mg during the firstmonth and 5 mg the two following months) N=15 (8 restrictive type AN [AN-R] and7 bulimic-purging type AN [AN-BP]) vs. CBT-placebo, N=15 (10 AN-R and 5 AN-BP). There were no significant differences between the two groups in BMI or in theEDI questionnaire score. However, AN-BP treated with CBT-olanzapine improvedthe BMI score significantly (p=0.01) as compared with other groups. Both groupsshowed significant improvement in The Yale Brown Cornell for Eating DisorderRating Scale (p=0.08) score. Differences were not significant upon stratification of thegroups. Both groups obtained a significant in the measurement of aggressiveness(CBT-olanzapine: p=0.006 vs. CBT-placebo: p=0.05) and depression (CBTolanzapine:p=0.01 vs. CBT-placebo: p=0.01). Upon stratification of the groups, AN-BP treated with CBT-olanzapine obtained better results in aggressiveness (p=0.05)than AN-R. There were no differences between these groups in terms of depression.RCT1++RCT1++160CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

The CBT-olanzapine group obtained better results in the TCI questionnaire (TheTemperament and Character Inventory) (p=0.007) as compared with placebo. Uponstratification of AN-R treated with CBT-olanzapine, this type of AN obtained betterresults than the other groups (p=0.04). The concentration of hemovallinic acidincreased significantly in the group treated with CBT-olanzapine. There was nocorrelation between the concentration of hemovallinic acid and psychopathologicalparameters. Pharmacological treatment may improve significantly specific aspects ofAN.An RCT (Brambilla, 2007; Italy)319 comprised of 20 women with ANreceiving outpatient treatment (mean age: 23 years) compared CBT-nutritionalrehabilitation programme-olanzapine (N=10) vs. CBT-nutritionalrehabilitation programme-placebo (N=10) administered over 3 months(olanzapine: 2.5 mg 1 month and 5 mg 2 months). BMI increased significantlyin both groups but without differences between them. Leptine and ghrelineconcentrations did not change throughout the treatment course and nocorrelation was observed between plasma levels and BMI. Data suggest thatthe increase in BMI of subjects treated with olanzapine cannot be attributed tothe administration of this drug. Leptine and ghreline secretion was notaccountable for such changes.An RCT (Walsh, 2006; USA) 320 , comprised of a group of patients with AN (N=93)with a minimum BMI of 19.0 in a day hospital, compared CBT-fluoxetine (N=49) vs.CBT-placebo (N=44) over one full year. A similar percentage of patients from bothgroups (fluoxetine: 26.5% vs. placebo: 31.5%; p=0,57) maintained the BMI score(≥18.5) and continued in the study for a further 52 weeks. There were no significantdifferences in relapse time between both groups. (p=0.64). This study failed to showthat treatment with fluoxetine benefits patients with AN after recovery of bodyweight.RCT1++RCT1++9.16.2. Bulimia nervosa9.16.2.1. What is the efficacy of combined interventions in patients withBN?The answer is based on the NICE CPG (2004) 30 , which describes the results yielded byRCT according to variables of interest and in the high-quality SRSE (1++) elaborated by theAHRQ of the US (2006) 31 and in a more recent publication (Shapiro, et al. 2007) 211 . The updatedsearch has not identified any new evidence.In the case of BN, there are some RCTs that compare treatment with antidepressantsagainst a combination of antidepressants and psychological therapy. Other RCTs also comparesingle psychological therapy against a combination of single psychological therapy andantidepressants.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS161

Antidepressants vs. antidepressants-psychological therapyVariables: reduction / remission of binge-eating and purgingThere is insufficient evidence to show that antidepressants (desipramine, fluoxetine,imipramine) differ from the combination of CBT-antidepressants with regard to remissionof binge eating episodes (5 RCTs; N=291; Leitenberg, 1994 321 ; Jacobi, 2002 322 ;Goldbloom, 1997 323 ; Agras, 1992 324 ; Walsh, 1997 233 ; randomised effects model RR: 1.29;95% CI: 0.99 to 1.69) and remission of purging episodes (5 RCTs; N=199; Leitenberg,1994 321 ; Jacobi, 2002 322 ; Goldbloom, 1997 323 ; Agras, 1992 324 ; Walsh, 1997 233 ; randomisedeffects model RR: 1.23; 95% CI: 0.93 to 1.64) at treatment completion.There is strong evidence to determine that the combination antidepressants-CBT vs.antidepressants (desipramine, fluoxetine) is suitable to reduce the frequency of bingeeatingepisodes (4 RCTs; N=133; Jacobi, 2002 322 ; Goldbloom, 1997 323 ; Agras, 1992 324 ;Walsh, 1997 233 ; SMD: 0.55; 95% CI: 0.21 to 0.90) but limited to reduce the frequency ofpurging episodes at treatment completion (5 RCTs; N=141; Leitengerg, 1994 321 ; Jacobi,2002 322 ; Goldbloom, 1997 323 ; Agras, 1992 324 ; Walsh, 1997 233 ; SMD: 0.49; 95% CI: 0.15 to0.83).There is insufficient evidence to show that antidepressants (desipramine, fluoxetine)differ from the combination of CBT-antidepressants with regard to remission andfrequency of binge eating episodes (2 RCTs; N=81; Jacobi, 2002 322 ; Agras, 1992 324 ; RR:1.12; 95% CI: 0.88 to 1.42), (1 RCT; N=21; Agras, 1992 324 ; SMD: 0,29; 95% CI: -0.58 to1.15), respectively, and in the remission and frequency of purging episodes (3 RCTs;N=95; Leitenberg, 1994 321 ; Jacobi, 2002 322 ; Agras, 1992 324 ; RR: 1.10; 95% CI: 0.87 to1.39), (2 RCTs; N=29; Leitenberg, 1994 321 ; Agras, 1992 324 ; SMD: 0.46; 95% CI: -0.31 to1.23) at post-treatment follow up, respectively.There is insufficient evidence to show that antidepressants (fluoxetine) differ from thecombination of SH-antidepressants with regard to remission and frequency of bingeeatingepisodes (1 RCT; N=47; Mitchell, 2001 258 ; RR: 1.11; 95% CI:0.83 to 1.48), (1RCT; N=34; Mitchell, 2001 258 ; SMD: 0.37; 95% CI: -0.24 to 0.97) and remission andfrequency of purging episodes (1 RCT; N=47; Mitchell, 2001 258 ; RR:1.11; 95% CI: 0.83to 1.48), (1 RCT; N=34; Mitchell, 2001 258 ; SMD: 0.31; 95% CI:-0.29 to 0.91)respectively, at treatment completion.There is insufficient evidence to show that antidepressants (desipramine) differ from thecombination de SFP-antidepressants with regard to remission and frequency of bingeeating episodes (RR: 0.95; 95% CI: 0.75 to 1.21), (SMD: -0,29; CI 95%: -0.85 to 0.27)and remission and frequency of purging episodes (RR: 0.95; 95% CI:0.75 to 1.21 andSMD: 0.26; 95% CI: -0.30 to 0.83) respectively at treatment completion according to 1RCT (N=50; Walsh, 1987) 288 .Variable: depressionThere is insufficient evidence to show that the combination of CBT-antidepressantsRCT1++RCT1++RCT1++RCT1++RCT1++RCT1++162CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

(desipramine, fluoxetine) differs from antidepressants alone in depression scores (4RCTs; N=125; Jacobi, 2002 322 ; Goldbloom, 1997 323 ;Agras, 1992 324 ; Walsh, 1997 233 ; SMD:0.31; 95% CI: -0.05 to 0.66) and in generalized psychiatric symptoms (2 RCTs; N=85;Jacobi, 2002 322 ;Walsh, 1997 233 ; SMD: 0.10; 95% CI: -0.33 to 0.53) at treatmentcompletion.There is insufficient evidence to show that treatment with antidepressants (desipramine)differs from SFP-antidepressants with regard to the score obtained on depression (SMD:0.26; 95% CI: -0.30 to 0.83) and in generalized psychiatric symptoms (SMD: -0.22; 95%CI: -0.78 to 0.34) at treatment completion according to 1 RCT (N=50; Walsh, 1997) 233 .RCT1++Psychological Therapy vs. Antidepressants-PsychologicaltherapyVariables: reduction / remission of binge-eating andpurgingThere is insufficient evidence to show that CBT differs from combination of CBTantidepressants(desipramine, fluoxetine, imipramine) with regard to remission andfrequency of binge-eating (5 RCTs; N=225; Jacobi, 2002 322 ; Agras, 1992 324 ; Walsh,1997 233 ; Fichter, 1991 295 ; Goldbloom, 1997 323 ; randomised effects model RR:1.09; 95% CI:0.83 to 1.42), (5 RCTs; N=185; Jacobi, 2002 322 ; Agras, 1992 324 ; Walsh, 1997 233 ; Fichter,1991 295 ; Goldbloom, 1997 323 ; SMD: 0.38; 95% CI: 0.09 to 0.68) and remission of purgingepisodes (5 RCTs; N=199; Jacobi, 2002 323 ; Agras, 1992 324 ; Walsh,1997 233 ; Leitenberg,1994 321 ; Goldbloom, 1997 323 ; RR: 0.94; 95% CI: 0.69 to 1.28) at treatment completion.There is insufficient evidence to show that CBT differs from the combination CBTantidepressants(desipramine, fluoxetine) with regard to remission and frequency of bingeeating episodes (2 RCTs; N=84; Jacobi, 2002 322 ; Agras, 1992 324 ; RR: 0,86; 95% CI:0.64 to1.14), (1 RCT; N=32; Agras, 1992 324 ; SMD: -0.19; 95% CI: -0.94 to 0.56) and remissionof purging episodes (3 RCTs: N=98; Jacobi, 2002 322 ; Agras, 1992 324 ; Leitenberg,1994 321 ;RR: 0.87; 95% CI: 0.68 to 1.13), (2 RCTs; N=43; Leitenberg, 1994 321 ; Agras 1992 324 ;SMD: -0.27; 95% CI: -0.90 to 0.37) at post-treatment follow up.There is insufficient evidence to show any differences between SH vs. SH-antidepressants(fluoxetine) with regard to remission and frequency of binge eating episodes (1 RCT;N=43; Mitchell, 2001 258 ; RR: 1.01; 95% CI: 0.73 to 1.41), (1 RCT; N=40; Mitchell,2001 258 ; SMD: 0.20; 95% CI: -0.43 to 0.82) and remission and frequency of purgingepisodes (1 RCT; N=43; Mitchell 2001 258 ; RR: 1.01; 95% CI: 0.73 to 1.41), (1 RCT;N=40; Mitchell, 2001 258 ; SMD: 0.36; 95% CI: -0.27 to 0.98) at treatment completion.There is insufficient evidence to show that SFT-antidepressants (desipramine) differsfrom SFT alone with regard to remission and frequency of binge-eating episodes (RR:1.00; 95% CI: 0.73 to 1.38; SMD: -0.07; 95% CI: -0.66 to 0.52) and in remission andfrequency of purging episodes (RR: 1.05; 95% CI: 0.85 to 1.30; SMD: 0.25; 95% CI: -0.35 to 0.84) at treatment completion according to 1 RCT (N=44; Walsh, 1997) 233 .RCT1++RCT1++RCT1++RCT1++163CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

There is insufficient evidence to show that NC differs from its combination withantidepressants (fluoxetine) with regard to remission and frequency of binge-eatingepisodes (1 RCT; N=67; Beumont, 1997 294 ; RR: 0.97; 95% CI: 0.62 to 1.54), (1 RCT;N=65; Beumont, 1997 294 ; SMD: -0.17; 95% CI: -0.66 to 0.31) and in remission andfrequency of purging episodes (1 RCT; N=77; Beumont, 1997 294 ; RR: 0.97; 95% CI: 0.62to 1.54), (1 RCT; N=65; Beumont, 1997 294 ; SMD: 0.34; 95% CI: -0.15 to 0.84) attreatment completion.There is insufficient evidence to show that NC differs from its combination withantidepressants (fluoxetine) with regard to remission and frequency of binge-eatingepisodes (1 RCT; N=67; Beumont, 1997 294 ; RR: 0.70; 95% CI: 0.50 to 0.97; NNT: 4; 95%CI: 3 to 25), (1 RCT; N=40; Beumont, 1997 294 ; SMD: -0.08; 95% CI: -0.71 to 0.54) and inremission and frequency of purging episodes (1 RCT; N=67; Beumont, 1997 294 ; RR: 0.70;CI 95%: 0.50 to 0.97; NNT: 4; 95% CI: 3 a 25), (1 EC; N=40; Beumont, 1997 294 ; SMD:-0.05; 95% CI: -0.68 to 0.58) at treatment completion.RCT1++RCT1++Variable: depressionThere is insufficient evidence to show that CBT-antidepressants (desipramine, fluoxetine)differ from CBT alone with regard to depression (5 RCTs; N=179; Fichter,1991 295 ; Jacobi,2002 322 , Goldblomm, 1997 323 ,Agras, 1992 324 ,Walsh, 1997 233 ; SMD: 0.18; 95% CI: -0.12 to0.48) and generalised psychiatric symptoms (2 RCTs; N=85; Jacobi,2002 322 ; Walsh,1997 233 ; SMD: -0.09; 95% CI: -0.52 to 0.34) at treatment completion.There is insufficient evidence to show SFT-antidepressants (desipramine) differs fromSFT alone with regard to depression (SMD: 0.37; 95% CI: -0.22 to 0.97) and generalisedpsychiatric symptoms (SMD: 0.00; 95% CI: -0.59 to 0.59) at treatment completion,according to 1 RCT (N=44; Walsh, 1997) 233 .There is insufficient evidence to show that NC differs from its combination withantidepressants (fluoxetine) in depression at treatment completion (1 RCT; N=67;Beumont, 1997 294 ; SMD: 0.25; 95% CI: -0.23 to 0.73) and in the follow up after treatment(1 RCT; N=40; Beumont, 1997 294 ; SMD: 0.30; 95% CI: -0.34 to 0.93).RCT1++RCT1++RCT1++Other resultsAn RCT (Goldbloom, 1997; Canada) 323 compared fluoxetine (60 mg/day) vs. CBT vs.fluoxetine (60 mg/day)-CBT in 60 adult women with BN receiving outpatient treatment for 12weeks. At 12 weeks no differences were found among the groups in the measurements relating tofeeding. The 3 interventions improved the main bulimic symptoms. The combination (fluoxetine60mg/day-CBT) and CBT alone achieved better results than fluoxetine alone to reduce bingeeatingand purging episodes, both subjective and objectively, as well as thoughts relating toabstinence or remission.The scores achieved in the depression scale and the weight did not show any differences amongthe 3 groups.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS164

An RCT (Walsh, 2004; USA) 328 compared fluoxetine vs. placebo vs. GSH vs. fluoxetine-GSH in 91 adult women diagnosed with BN undergoing outpatient BN. Fluoxetinealone and in combination with GSH achieved better results to reduce purging, bingeeating,food restriction and depression than those observed in other groups.An RCT (Mitchell, 2001; USA) 258 compared fluoxetine vs. placebo vs. SH vs.fluoxetine-SH in 91 adult women with BN receiving outpatient treatment. Fluoxetinewas associated with a higher decrease in the number of purging episodes as comparedto placebo, but not so in the number of binge-eating episodes. There are no significantdifferences in depression, and neither in remissions nor abstinence.In 2 RCTs (Agras, 1992; USA324 and Agras, 1994325) compared desipramine (for 16weeks) vs. desipramine (24 weeks) vs. desipramine-CBT (16 weeks) vs. desipramine-CBT (24 weeks) vs. CBT alone (24 weeks) in 71 adult women with BN undergoingoutpatient treatment. The combined treatment of 16 and 24 weeks was more effectivethan desipramine alone to decrease binge-eating and purging episodes. The combinedtreatment of 24 weeks was more effective in the patient’s concerns over the diet and thefeeling of hungriness. There were no differences in remission or abstinence, neither inthe weight. Depression was not reported. At one year follow up, the 24 weekcombination and CBT alone were better than the 16 week combination anddesipramine alone to reduce the number of binge-eating and purging episodes. Of thepatients who presented remission or abstinence at treatment completion, between 78%and 100% maintained the effect at the 1 year follow up. This was only observed incases in which treatment had been combined.2 RCTs (Walsh, 1997 233 ; Wilson, 1999 326 ) compared CBT-placebo vs. CBT-desipraminealone or desipramine and afterwards fluoxetine vs. support therapy-placebo vs. supporttherapy-medication (desipramine alone or desipramine followed by fluoxetine) vs.medication alone (desipramine alone or desipramine followed by fluoxetine)administered over 16 weeks to 120 adult women with BN undergoing outpatienttreatment. In analysing all the groups that included CBT vs. all the groups that includedsupport therapy, it was observed that CBT was better to reduce the frequency of bingeeatingand purging episodes. The combinations of CBT + medication were superior toCBT alone to reduce the frequency of binge-eating episodes, EAT scores, depression,weight and to increase the number of remissions. The combinations of CBT andmedication were superior to medication alone to reduce the frequency of binge-eatingepisodes, EAT scores, body image and to increase the number of remissions.Medication alone was superior to CBT alone to reduce BMI and weight. Medicationalone was superior to IPT-medication to reduce the frequency of binge-eating andpurging episodes. Medication was superior to lessen depression. CBT was notassociated with a greater probability for remission.An RCT (Mitchell, 2002) 327 compared IPT vs. fluoxetine (16 weeks) vs. fluoxetine (8weeks)-desipramine (8 weeks) in 62 adult women diagnosed with BN receivingoutpatient care. No differences were noted in any of the dietary or psychologicalaspects.RCT1++RCT1+RCT1+RCT1++RCT1+165CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Summary of the EvidenceSRSE 311++SRSE 311++SRSE 311++SRSE 311++The above mentioned RCTs show preliminary evidence of the most suitablecombinations between psycho-drugs and behavioural psychological therapies.The studies have different designs and there is no repetition of their results.Hence, more studies are needed in order to be able to evaluate and ascertaintheir efficacy.CBT and the combination CBT-fluoxetine afford better results than treatmentwith fluoxetine alone to reduce binge-eating and purging at treatmentcompletion (Goldbloom, 1997) 323 .Within the context of special programmes for EDs, both fluoxetine as well asSH therapies (guided or not) are better to reduce purging. Nonetheless, thecombination of both therapies does not increase treatment efficacy (Mitchell,2001) 258 .The treatment of affected individuals who do not respond to behaviouralpsychological therapies continues to pose a limitation to the current evidence.(Mitchell, 2002) 327 .9.16.2.2. What is the safety of combined interventions in patients with BN?The answer is based on the NICE CPG (2004) 30 and on the high-quality SRSEs (1++), oneelaborated by the AHRQ of the US (2006) 31 and the more recent one elaborated by Shapiro, etal. (2007) 211 . The updated search has not identified any new evidence. Question 9.16.1.1.describes the studies briefly.Scientific EvidenceThere is insufficient evidence to determine if there are any significant clinicaldifferences in the number of withdrawals for any given reason between treatment withantidepressants vs. CBT-antidepressants (desipramine, fluoxetine, imipramine) (4 RCTs;N=206; Mitchell, 1990 243 ; Jacobi, 2002 322 ; Goldbloom, 1997 323 ; Leitenberg, 1994 321 ; RR:1.17; 95% CI: 0.81 to 1.68).There is insufficient evidence to determine if there are any significant clinicaldifferences in the number of withdrawals due to adverse effects between treatment withantidepressants (imipramine) vs. CBT-antidepressants (1 RCT; Mitchell, 1990 243 , N=106;RR: 0.64; CI 95%: 0.11 to 3.69).There is insufficient evidence to determine if there is a clinically significant differencebetween treatment with CBT vs. CBT-antidepressants (desipramine, fluoxetine,imipramine) in the number of withdrawals for any given reason (5 RCTs; N=230;Fichter, 1991 295 ; Jacobi, 2002 322 ; Goldbloom, 1997 323 ; Mitchell, 1990 243 ; Leitenberg,1994 321 ; RR: 0.70; 95% CI: 0.45 to 1.08).RCT1++RCT1++RCT1++166CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

There is insufficient evidence to determine if there is a clinically significant differencebetween the treatment with CBT and the combination of CBT-antidepressants(imipramine) in the number of withdrawals due to adverse effects (1 RCT; N=86;Mitchell, 1990 243 ; RR: 0.51; 95% CI: 0.06 to 4.70).There is insufficient evidence to determine if there is a clinically significant difference inthe treatment with antidepressants (fluoxetine) vs. fluoxetine-SH regarding the numberof withdrawals for any given reason at treatment completion (2 RCTs; N=91; Mitchell,2001 258 ; Walsh 2004 328 ; RR: 1.15; 95% CI: 0.72 to 1.84).There is insufficient evidence to determine whether treatment with SH vs. SHantidepressants(imipramine) differs in the number of withdrawals for any given reason(1 RCT; N=43; Mitchell, 1990 243 ; RR: 0.48; 95% CI: 0.05 to 4.88).There is insufficient evidence to determine whether treatment with NC differs fromtreatment with NC-antidepressants (fluoxetine) in the number of withdrawals for anygiven reason at treatment completion (RR=0.66; 95% CI: 0.29 to 1.49) or due to adverseeffects (RR: 0.11; 95% CI: 0.01 to 2.04) according to 1 RCT (N=67; Beumont, 1987) 294 .An RCT (Goldbloom, 1997) 323 compared fluoxetine vs. fluoxetine-CBT. There were 2withdrawals due adverse effects in the fluoxetine group and four in the combinationfluoxetine-CBT.In an RCT (Walsh, 2004) 328 , there was a 54% withdrawal rate in the group treated withfluoxetine-GSH vs. 88% in the group treated with placebo-GSH vs. 70% in the grouptreated with fluoxetine vs. 64% in the placebo group. Adverse effects were not reported.In an RCT (Mitchell, 2001) 258 , the number of withdrawals was low: placebo (5%),fluoxetine (0%), placebo-SH (0%), fluoxetine-SH (5%). No adverse effects werereported.In 2 RCTs (Agras, 1992 324 ; Agras, 1994 325 ), no information was reported regardingadverse effects. The mean withdrawal rate was 25%.In 2 RCTs (Walsh, 1997 233 ;Wilson, 1999 326 ), the mean withdrawal rate was 34%, and noinformation was provided on adverse effects.In an RCT (Mitchell, 2002) 327 , no information was provided on adverse effects. Thepercentage of withdrawals was 32% in the IPT group and 48% in the antidepressantsgroup.RCT1++RCT1++RCT1++RCT1++RCT1+RCT1++RCT1+RCT1+RCT1++RCT1+Summary of the EvidenceCPG30When these therapies were implemented in primary care, the number ofwithdrawals in the group treated wit fluoxetine was 70%, higher than the 54%observed in the group treated with fluoxetine-GSH (Walsh, 2004) 328 .167CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

9.16.3. Binge-eating disorder9.16.3.1. What is the efficacy of combined interventions in patients withBED?The answer is based on NICE CPG (2004) 30 , which describes the results yielded by RCTs,and on the high-quality SRSEs (1++), one elaborated by the AHRQ of the US (2006) 31 and themore recently published one conducted by Brownley, et al. (2007) 245 . The updated search hasidentified one new RCT.Scientific EvidenceAn RCT (Grilo, 2005; USA) 329 compared fluoxetine (60 mg/day) vs. placebo vs. CBT vs.CBT-fluoxetine in 108 adult patients (78% women) diagnosed with BED and treated onan outpatient basis for 16 weeks. The groups that received CBT (alone or in combinationwith fluoxetine) achieved better results than the placebo and the fluoxetine alone groupsto reduce the frequency of binge-eating episodes, ED-related symptoms, depression, andgreater frequency of remission. There were no differences with regard to weight.An RCT (Agras, 1994; USA) 325 compared CBT (3 months) – weight loss therapy (6months) –weight loss therapy (9 months) vs. CBT (3 months) – weight loss therapy (6months) - desipramine (300 mg/day) in 109 adult women with BED on an outpatientbasis. The groups that received CBT experienced a significant in the binge-eatingepisodes after 12 weeks of treatment, even though the effect was not maintained at the 1year follow up. There were no differences regarding depression scores among thegroups. At treatment initiation, the weight loss was greater in the group receiving weightloss therapy. At the 3-month follow up, the weight loss was greater in the CBTdesipraminegroup (mean weight loss: 4.8 Kg).An RCT (Grilo, 2005; USA) 330 compared CBT-orlistat (120 mg 3/day) vs. CBT-placeboover12 weeks of treatment in 50 adult patients (88% women) (BMI>30) with BEDundergoing outpatient treatment. The group on orlistat had a greater remission rate attreatment completion, but not so at the 2-month follow up. This group also experiencedweight loss.An RCT (Devlin, 2007; USA) 331 comprised of 116 people suffering from BED (90females and 26 males) (age range: 18-70 years) compared individual CBT- fluoxetinevs. individual CBT over 5 months with a follow up at +2 years. Both groups showed animprovement in the frequency of the binge-eating episodes and their remission after 2months of treatment. The odds ratio (odds at 24months/ post-treatment) for remission ofthe binge-eating episodes at 2 years after treatment was 1.373 times the odds atcompletion of 5 months of treatment. Subjects who received individual CBTexperienced a greater reduction in the frequency of binge-eating episodes and greaterremission odds ratio of such episodes as compared to the subjects who had not receivedthis therapy at 2 years. There were no differences regarding weight in neither of thegroups. The group that received fluoxetine achieved better results in the reduction ofdepressive symptoms at 2 years. A short-term treatment may show benefits in the longterm and not all treatments are equivalent in terms of the benefits they provide.RCT1++RCT1+RCT1++RCT1++168CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Summary of the EvidenceRSEC 31 The combination of pharmacological treatment with CBT can reduce the1++ occurrence of binge-eating episodes and improve weight loss. However, nodefinition has yet been provided as to what the best medication is to maintain theweight loss. Moreover, there are no empiric data on what the ideal treatmentduration might be to maintain BED remission and weight loss.9.16.3.2. What is the safety of combined interventions in patients withBED?The answer is based on NICE CPG (2004) 30 , on the quality SRSE (1++) elaborated by theAHRQ of the US (2006) 31 and on other more recently published publication conducted byBrownley, et al. (2007) 245 . Question 9.16.3.1. describes the studies briefly.Scientific EvidenceIn an RCT (Grilo, 2005; USA) 329 that compared fluoxetine vs. placebo vs. CBT-placebovs. CBT-fluoxetine, the percentage of withdrawals was as follows: placebo (15%),fluoxetine (22%), CBT-placebo (21%), CBT-fluoxetine (23%). No information wasprovided on adverse effects.In an RCT (Agras, 1994) 325 , the withdrawal rate from weight loss therapy was 27%, fromCBT-weight loss therapy it was 17%, and from CBT- weight loss therapy-desipramine itwas 23%. Eight subjects stopped taking desipramine due to adverse effects.An RCT (Grilo, 2005) 330 compared CBT-orlistat (120 mg 3/day) vs. CBT-placebo for 12weeks of treatment in 50 adult patients (88% women) (BMI>30) with BED receivingtreatment on an outpatient treatment basis. The number of withdrawals was as follows:orlistat-CBT (24%); placebo-CBT (20%). The group treated with orlistat-CBT had moregastrointestinal adverse effects.RCT1++RCT1+RCT1++169CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

TREATMENT OF EATING DISORDERS THATOCCUR WITH COMORBIDITIES9.17. What is the treatment for eating disordersthat occur with mental disorders?The mental disorders most frequently associated with eating disorders are: substance-relateddisorders, anxiety disorders, OCD, personality disorders, mood disorders and impulse controldisorders.Information on treatment in the presence of these associations has been extracted from theNICE guide (2004) 30 , although it only establishes recommendations for certain associations.Scientific EvidenceThere are special programmes (that have not been sufficiently assessed) for patients withBN associated with substance abuse, self-inflicted injuries and/or BPD.The presence of impulse control disorder or personality disorder (type B) in patientswith BN is associated with poor treatment outcomes.Care must be exercised when using medication to treat comorbid conditions such asdepression and OCD compulsive symptomatology in patients with AN when theseclinical pictures could be resolved through weight gain.CPG 30CPG 30CPG 309.18. What is the treatment for eating disordersthat occur with organic disorders?The organic disorders that are most frequently associated with eating disorders are:diabetes mellitus (DM), obesity, malabsorbtion syndromes and thyroid diseases.Information on treatment in the presence of these combinations has been extracted from theNICE guide 30 , although it only formulates recommendations for certain associations.Scientific EvidenceThe presence of type 1 DM requires changes in the psychological treatment of an eatingdisorder. In CBT-BN, control over eating is very important and can clash with NCaimed at diabetics (Peveler, 1993 332 ). There are special guidelines that adapt CBT-BN totype 1 DM.CPG 30170CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

RecommendationsD 9.18.1. Treatment in clinical and subclinical cases of eating disorders in patientswith DM is essential due to the increased risk presented by this group.(Adopted from recommendation 7.5.8.1. of the NICE guide).D 9.18.2. Patients with Type 1 DM and an eating disorder must be monitored due tothe high risk of developing retinopathy and other complications. (Adoptedfrom recommendation 7.5.8.2. of the NICE guide).D 9.18.3. Young people with Type 1 DM and poor adherence to antidiabetictreatment should be assessed for the probable presence of an eatingdisorder. (Adopted from recommendation 5.2.5.5. of the NICE guide).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS171

TREATMENT OF CHRONIC EATING DISORDERS9.19. How are chronic eating disorders treated?Tertiary prevention aims to resolve the most serious symptoms, palliate the most severecomplications and avoid vital risk in chronic cases, which have generally been refractory totreatment and in which expectations of remission are low or inexistent.In chronic eating disorders, tertiary prevention includes management of the organic(cachexia, electrolyte imbalance, immune deficiency, etc.) and mental (loss of impulse control,risk of self-aggression, suicide prevention, etc.) state, maintenance pharmacological treatment,behavioural pact within the family (acceptance of certain behaviours and reaching agreement onothers, indications for the family to identify relapse in maladaptive symptoms, etc.) and socialreinsertion measures in which family, health care resources and support associations for patientswith eating disorders and their family members play a very important role.There is no evidence on the effect of different interventions aimed at chronic eatingdisorder cases.Tertiary prevention of eating disorders was not addressed in the NICE CPG (2004) 30 . Fourof the documents 10, 16, 19, 147 elaborated in our setting formulate recommendations on this aspect andbased on them the working group has formulated the recommendations for its approach.Recommendations 9.19.1. The health care professional in charge of the care of chronic eatingdisorder cases should inform the patient on the possibility of recovery andadvise him/her to see the specialist regularly regardless of the number ofyears elapsed and previous therapeutic failures. 9.19.2. It is necessary to have access to health care resources that are able toprovide long-term treatments and follow-up on the evolution of chroniceating disorder cases, as well as to have social support to decrease futuredisability.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS172

TREATMENT OF EATING DISORDERS INSPECIAL CASES9.20. What is the treatment for eating disorders inspecial situations such as pregnancy and delivery?Evidence on the considerations that should be acknowledged when the patient is pregnant orgiving birth has been extracted from the NICE guide (2004) 30 .Summary of the EvidenceCPG 30CPG 30CPG 30CPG 30CPG 30Pregnancy with purging practices or pregnancy with overweight or obesity inan eating disorder is specific risk situations. Delivery can also be considered arisk situation that can lead to the onset of an eating disorder (Crow, 2008 333 ;Franko, 1993 334 ; Fairburn, 1990 335 ).In a follow-up study of patients with AN (N=140), fertility was reduced by athird of what was expected, prematurity doubled and perinatal mortality was sixtimes greater than in people without an eating disorder (Brinch, 1988) 336 .In another follow-up study of 66 pregnant women with AN, these patientspresented a higher percentage of C-sections and prematurity than the groupwithout eating disorders (Bulik, 2008) 337 .In a study conducted on pregnant women with AN, monitoring of the foetus’weight was performed. The foetus’s growth was slow, especially in the lasttrimester (Treasure, 1988) 338 .Pregnant women with AN have high risk of presenting premature deliveries.There are case-series that suggest the difficulties encountered by women withAN to feed their infants (Russell, 1998 339 ; WezelMeijle, 1989 340 ), while otherstudies report abnormal growth of these children (Hodes, 1997) 341 .RecommendationsD 9.20.1. Pregnant patients with AN, whether it is the first episode or a relapse,require intensive prenatal care with adequate nutrition and follow-up offoetal development. (Adopted from recommendation 6.4.8.1. of the NICEguide).D 9.20.2. Pregnant women with eating disorders require careful follow-upthroughout pregnancy and the postpartum period. (Adopted fromrecommendation 7.5.10.1. of the NICE guide).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS173

10. Assessment of Eating DisordersKey Questions:10.1. What instruments are useful to assess eating disorder symptoms and behaviour?10.2. What instruments are useful for the psychopathological assessment of eating disorders?10.1. What instruments are useful to assess eatingdisorder symptoms and behaviour?In the past few years several instruments have been designed for the assessment of symptomsand behaviours presented by patients with eating disorders. Self-report questionnaires and semistructuredinterviews (see chapter 2, “Diagnosis”) are the two main assessment instruments.There are also other measures related to preoccupation with body image, dietary consumption,amongst others, as well measures related to comorbidity (depression, anxiety, etc.).Self-report questionnaires measure symptoms and risk behaviour of eating disorders, anddo not provide a specific diagnosis (see chapter 2, “Diagnosis”). In contrast to semistructuredinterviews that require experience and individualised administration and, hence, entail increasedcost and time, self-report questionnaire are relatively economical, require less time and can beapplied to big groups of people; however, there is greater difficulty as far as definition andinterpretation of concepts, which mandates caution in the generalisation of results 342 .When applying a questionnaire, it is important to borne in mind its psychometric properties:validity and reliability, sensitivity and specificity, amongst other characteristics, with the aim ofselecting the most convenient questionnaire in accordance with assessment objectives,throughout the initial diagnostic phase and also throughout the treatment phase.This chapter presents a review of different self-report questionnaires that are mostfrequently used in the assessment of eating disorders. Additionally, some instruments that areused to assess characteristics related with eating disorders but that are not per se instruments todetect/diagnose/assess eating disorders are mentioned. Instruments employed in thepsychopathological assessment of eating disorders are also described.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS174

10.1.1. Specific instruments for the assessment of eatingdisorders:EAT-40, EAT-26 and ChEATAdapted Spanish versions that have been validated in our setting are available.(See chapter 6, “Detection” and Annexes 2.2. to 2.4.)EDIEating Disorder Inventory. Garner, et al., 1983The EDI (or EDI-I) is a self-report instrument designed to assess different cognitive andbehavioural dimensions of AN and BN. It consists of 64 items grouped in 8 subscales that arepositively correlated. The first three subscales measure behaviour and attitudes toward food,weight and body image (drive for thinness, bulimic symptomatology, self body imagedissatisfaction), disturbances expressed in these areas are not specific of AN, given that similarresponses appear in groups of people who are concerned about their diet. The other fivesubscales (ineffectiveness and low self-esteem, perfectionism, interpersonal distrust,interoceptive awareness or identification and maturity fears) assess general psychologicalcharacteristics associated with eating disorders, which are fundamental aspects of AN 343 .Each item is scored using a 6-point Likert scale. All subscales can be added to obtain anoverall score or use each scale separately; clinically speaking, the quantitative value of each ofthe eight subscales is more relevant than the overall score. The maximum total score of thisquestionnaire is 192, the cut-off point is 42 points or less in the eight original subscales todiagnose an eating disorder. Some authors claim that the specificity of EDI is low, since itcannot properly differentiate individuals with eating disorders from those who present otherpsychological disorders. In a study carried out on women, it was reported that the subscales thatbest differentiate AN from BN are the ones addressing bulimic symptomatology and body imagedissatisfaction, although the latter is high in both eating disorders. On the other hand, subscalessuch as low self-esteem, interpersonal fears, maturity fears, interoceptive identification andmotivation to lose weight, which are usually high in both pathologies, distinguish patients withan eating disorder from control subjects. Subscales such as body image dissatisfaction,motivation to lose weight and dieting are usually high both in patients with eating disorders andin the general population 345 .There are several opinions on the utility of the EDI. Several authors suggest that it can beused as a screening test in non-clinical samples, but the fact that its ability to distinguishdifferent types of eating disorders is questionable must be taken into account. However, it issuggested that the EDI is able to discriminate individuals with eating disorders and individualswithout any psychiatric disturbances. This questionnaire has proven to be sensitive to changesregistered in individuals when treatment is applied.Spanish version of the EDIThe Spanish adaptation of the EDI was developed by Guimerá and Torrubia, 1987, in a clinicalsample (hospital) of 24 patients with AN and 24 control subjects sharing similar ages andsociodemographic characteristics 346 .CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS175

EDI-2 (Version 2 of the EDI-1)Later (1991), Garner, et al. developed the EDI-2, comprised of 91 items (64 items of the EDI-1and an additional 27 items). The items are grouped in 11 scales, 8 of them main scales(obsession about thinness, bulimia, body dissatisfaction, ineffectiveness, perfectionism,interpersonal distrust, interoceptive awareness and maturity fears) and 3 provisional scales (not apart of the EDI-1) (ascetism, impulse regulation and social insecurity). A 5th gradeeducational level is required to answer this self-report measure 347 .Spanish version of the EDI-2The Spanish version was adapted by the TEA publishing house 1998 348There is also a Spanish version validated in the Mexican population. When the cut-off point is80 for the overall score, sensitivity is 91% and specificity is 80%; when it is 105 points,sensitivity is 82% and specificity is 89% 349 .BULITBulimia Test. Smith and Thelen, 1984There is an adapted Spanish version validated in our setting. (see chapter 6, “Detection” andAnnex 2.5.)BITEBulimia Investigatory Test Edinburgh. Henderson and Freeman, 1987There is an adapted Spanish version validated in our setting. (see chapter 6, “Detection” andAnnex 2.6.)EDE-QEating Disorders Examination-questionnaire. Fairburn and Beglin, 1993The EDE-Q is a self-report questionnaire (it can be completed in less than 15 minutes) derivedfrom the EDE semistructured interview developed by Fairburn and Beglin, 1993, and whichcontains its three main subscales (restraint, weight concern and shape concern) 350 . Resultsindicate a consistent positive correlation, albeit moderate, between the EDE and the EDE-Q.Correlation was higher in characteristics that do not present definition difficulties (for example,frequency of self-induced vomiting or average –days per week- laxative abuse); the greatestdiscrepancy indexes were found in the days-per-week assessment in which binge-eating episodestook place. These values were consistently higher in the EDE-Q. There is no informationconcerning the adaptation and validation of the EDE-Q in the Spanish population. However,there is an adapted Spanish version in a Colombian population sample (S-EDE-Q) 351 .SCOFFSurvey Sick, Control, One, Fat, Food questionnaire. Morgan, et al., 1999There is an adapted Spanish version validated in our setting. (see chapter 6,“Detection” and Annex 2.1.)ACTA(Attitude Regarding Change in Eating Disorders) Beato and Rodríguez,2003The ACTA questionnaire was developed by L Beato and T Rodríguez, 2003 352 , with the objectiveCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS176

of assessing attitude regarding change in eating disorders. It consists of 59 items distributed in 6subscales: precontemplation, contemplation, decision, action, maintenance and relapse. TheACTA is an easily administered instrument with adequate reliability and validity, and its usewithin the motivational approach can contribute useful information relating to therapeuticprocess knowledge.ABOSAnorectic Behaviour Observation Scale for parents/spouse.Vandereycken, 1992.The ABOS is a self-report questionnaire developed to obtain information from family members(parents) on their children’s behaviours and attitudes that may be symptomatic of AN or BN.Using a cut-off point of 19 points, the ABOS obtained 90% sensitivity and 89.6% specificity ina sample of female students, values that were reliable based on subsequent clinical assessment.It can be a complementary instrument to eating disorder screening tools 353 .Spanish version of the ABOSThere is no information regarding the availability of an adapted version of the ABOS scalevalidated in our setting.10.1.2. Instruments with measures related with eating disordersOne of the most important features of eating disorders is the perception of body image. Thereare several tools available for its assessment, including: BSQ, BIA, BAT and BES. It is alsoimportant to evaluate eating disorders in terms of internalisation of cultural influences on theaesthetic body model (culture of thinness). To this end, the CIMEC and its revised version canbe used. Another aspect that needs to be assessed is eating restraint, diet, weight, physicalactivity, etc. To assess these aspects and others it is important to select the most reliable andvalid questionnaire, one that is also brief and specific to what it intends to measure.BSQBody Shape Questionnaire. Cooper, et al.,1987The BSQ is a self-report questionnaire that measures body dissatisfaction, the fear of becomingfat, self-devaluation due to physical appearance, the desire to lose weight and avoidance ofsituations in which physical appearance might draw others’ attention.It can also be a useful tool in the exploratory study of individuals who are at risk of developingan eating disorder, acknowledging that a body scheme disorder is only one of the symptoms ofthis pathology. It consists of 34 items and it is scored on a 1-to-6 Likert type scale, 34-204being the range of scores. An overall score (the sum of direct item scores) can be obtained and4 subscales can be derived: body dissatisfaction, fear of becoming fat, low self-esteem due toappearance and the desire to lose weight. The cut-off point for the overall score has beendetermined to be 105 354 .Spanish version of the BSQThe BSQ has been adapted and validated in our population by Raich, et al., 1996 355CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS177

BIABody Image Assessment. Collins, et al.,1991The BIA is a visual scale in which 7 figural stimuli of children and 7 figural stimuli of youngadolescents, both male and female, appear separately, representing the standard percentile curvesfor BMI in children, ranging from the representation of a very thin figure to an overweightfigure, with a score range of 1 (thinness) to 7 (obesity), with 0.5 point increments. The BIA canobtain an indicative discrepancy index between different “me’s” by subtracting the scoresobtained from the real me (for example, real-ideal) 356 .Spanish version of the BIASpanish version developed by Sánchez, 2005BATBody Attitude Test. Probst, 1995The BAT is a questionnaire that assesses a subjective dimension of body image, specifically adisturbance in the attitude towards one’s own body. This test is endorsed by good psychometricresults. Although it was initially conceptualised to assess body experience and attitude towardsone’s own body in patients with eating disorders, it has also been used in the non-pathologicalpopulation. The 20 items it is comprised of are grouped into three main factors: negativeappreciation of body size, loss of familiarity with one’s own body and general bodydissatisfaction 357 .Spanish version of the BATThere is a Spanish version adapted and validated in our setting by Gila, et al., 1999, in a sampleof 165 patients with eating disorders (79 AN and 86 BN) and 220 girls from the generalpopulation. Its results indicate adequate validity and reliability 358 .BESBody-Esteem Scale. Mendelson and White, 1982The BES is a self-report instrument comprised of 24 items that assess body self-esteem inchildren over the age of 7 with acceptable reading competence. It is a one-dimensional scalewith yes/no answers that gathers information regarding feelings and self-evaluation of one’sappearance and evaluations attributed to others about one’s appearance. The BES has acceptablereliability and validity 359 .Spanish version of the BESThere is a Spanish version adapted and validated in our setting by Sperber,et al., 2004 360CIMECQuestionnaire of Influences of the Aesthetic Body ModelToro, et al., 1994The CIMEC was designed to measure relevant cultural influences that contribute to triggering,facilitating or justifying weight loss, especially for aesthetic or social reasons. It is comprised of40 direct items than assess body image related anxiety, influence of social models and influenceof social situations. Answers are assessed on a scale of 1 to 3 points. A higher score reflectsgreater influence of social models. The highest possible score is 80 and the lowest is 0, with aCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS178

cut-off point of 23/24 points 89 . It was elaborated and validated in a sample of young Spanishfemales (59 anorectics and 59 control subjects), matched by age and social class. Thequestionnaire showed satisfactory internal consistency, as well as appropriate sensitivity (81.4%)and specificity (55.9%), making it a possibly useful screening instrument given the relationshipbetween AN and sociocultural influences.CIMEC-26 (abbreviated version of the CIMEC)When the CIMEC-40 was assessed in both a clinical group and a control group, 26 items thatpresented statistically significant differences were alienated. These questions were used tocreate the CIMEC-26, from which 5 dimensions are derived: body image distress, mass mediainfluence, influence of verbal messages, influence of social models and influence of socialsituations.Results indicate that the CIMEC (CIMEC-40 and CIMEC-26) is a valid and reliableinstrument to assess the influence of aesthetic body models in the Spanish population by meansof certain specific sources (mass media, social models and social situations).CIMEC-12 (CIMEC version for prepubertal children)Spanish version developed by T Saucedo, 2000 361RecommendationsD 10.1.1. Assessment of patients with eating disorders should be comprehensive andinclude physical, psychological and social aspects, as well as a completeassessment of risk to self. (Adopted from recommendation 2.8.1.1. of theNICE guide).D 10.1.2. The therapeutic process modifies the level of risk for the mental andphysical health of patients with eating disorders, and thus should bemonitored throughout treatment. (Adopted from recommendation 2.8.1.2.of the NICE guide).D 10.1.3. Throughout treatment, health care professionals who evaluate children andadolescents with eating disorders should be alert to possible indicators ofabuse (emotional, physical and sexual) to ensure an early response to thisproblem. (Adapted from recommendation 2.8.1.3. of the NICE guide).D 10.1.4. Health care professionals who work with children and adolescents witheating disorders should familiarise themselves with national CPGs andcurrent legislation regarding confidentiality. (Adapted fromrecommendation 2.8.1.5. of the NICE guide).CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS179

10.1.5. The use of questionnaires adapted and validated in the Spanish populationis recommended for assessment of eating disorders.At present, the following specific instruments for eating disorders arerecommended: EAT, EDI, BULIT, BITE, SCOFF, ACTA and ABOS(version selection based on the patient’s age and other application criteria).To assess aspects related with eating disorders, the followingquestionnaires are recommended: BSQ, BIA, BAT, BES and CIMEC (theselection of the version should be based on age and other applicationcriteria).10.2. What instruments are useful for thepsychopathological assessment of eating disorders?(See also chapter 7, “Diagnosis”)10.2.1. ImpulsivenessBIS-11Barratt Impulsiveness Scale, version 11. Patton, et al., 1995The BIS-11 is a self-report survey used to assess impulsiveness. It consists of 30 items groupedinto four subscales: cognitive impulsiveness, motor impulsiveness, non-planned impulsivenessand total impulsiveness. These scales are scored using a 4-point Likert scale. The total score ofthe BIS-11 is a valid and reliable measure of impulsiveness. There are no cut-off points,although a distribution median has been proposed 362 .Spanish version of the BIS-11There is a Spanish version adapted and validated in our setting by M Oquendo,et al., 2001 363 .10.2.2. AnxietySTAIState-Trait Anxiety Inventory. Spielberger, et al., 1970The STAI is a self-report assessment of anxiety as a transitory state (anxiety/state; A/S) and asa latent trait (anxiety/trait; A/T). It can be applied to adolescents (aged 13 and over) and adults.The instrument consists of two parts comprised of 20 questions each. The first section (A/S)assesses a transitory emotional state, characterised by subjective, consciously perceived feelingsof tension and apprehension and by hyperactivity of the autonomous nervous system. Thesecond section (A/T) denotes relatively stable anxiety proneness and characterises individualswith a tendency to perceive situations as threatening. It has adequate validity and reliability 364 .CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS180

Spanish version of the STAIThere is a Spanish version adapted to our setting by TEA Publishing House, 1982 365Children version of the STAI (STAI-C)The STAI-C can be administered to children aged 9 to 15 years and takes 15 to 20 minutes. Itsobjective is the assessment of anxiety-state and anxiety-trait in this age group 366 .Spanish version of the STAI -CThere is a Spanish version adapted to our setting by TEA Publishing House, 1990 367HARSHamilton Anxiety Rating Scale. Hamilton, 1959The HARS is a hetero-administered scale used to assess anxiety by evaluating anxiety, tension,neurovegetative and somatic symptoms. The scale consists of 14 items with values rangingfrom 0 to 4 and determines the intensity of the symptoms it describes in the past month 368 .Spanish version of the HARSThere is a Spanish version that has been adapted to our setting by A Lobo and L Chamorro,2002 369 .CETA - Assessment of Anxiety Disorders in Children andAdolescentsEzpeleta, et al.Spanish original version developed by L Ezpeleta 37010.2.3. DepressionBDI or BeckBeck Depression Inventory. Beck, et al.,1961The BDI o Beck Depression Inventory is a self-report questionnaire used to assess the existenceor severity of depressive symptoms. Given its proven validity and reliability both in clinical andnon-clinical populations it is one of the most widely used tests. It is also useful in the screeningof the general population and somatic patients. It is comprised of 21 items and its objectives areto identify typical symptoms of severe depression and estimate depression severity. The overallscore is used to estimate depression severity. The score obtained ranges from 0 to 63 points andthe cut-off points are as follows: 0-9 (normal), 10-18 (mild depression), 19-29 (moderatedepression) and 30-63 (severe depression). It can be used in patients aged 16 and over 371 .Spanish version of the BDI or Beck depressionThere is an adapted version that has been validated for the Spanish population by C Conde andE Useros, 1975 372 . J Sanz, et al., 2003, later adapted the Beck-II (BDI-II) 373 .HAM-DHamilton Depression Rating Scale. Hamilton, 1959The HAM-D is a hetero-administered questionnaire that assesses the severity of depressivesymptoms, such as insomnia, agitation, anxiety and weight loss. Since its initial publication isCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS181

has been widely used. It consists of 21 multiple choice items. The first 17 questions contributeto the total score, while questions 18 to 21 provide more information on depression such as, forexample, the presence of paranoid symptoms in the patient 368, 374 .Spanish version of the HAM-DThere is a Spanish version adapted to our setting by A Lobo and L Chamorro, 2002 369 .CDIChildren Depression Inventory. Kovacs, 1991The CDI is the most widely used questionnaire and is highly endorsed by experts in childdepression, since it has proven to be very solid from a psychometric point of view and veryuseful for clinical purposes. It can be applied both in the general and clinical populations. In thefirst case, it is used for screening and in the second it constitutes the first element of diagnosis.The general depression score obtained is comprised of two scales: dysphoria and negative selfesteem.It is a self-report scale that contains 27 items. Each item has three possible answersthat are quantified on a range of 0 to 2, based on the absence or severity of symptoms. Thisquestionnaire can be administered to a population aged 8 to 15 years, with a completion time of10 to 25minutes 375.Spanish version of the CDIThere is a Spanish version, adapted by TEA Publishing House 37610.2.4. PersonalityMCMI-III – Millon Clinical Multiaxial InventoryMillon, 1990This tool enables the assessment and identification of patients with emotional and personaldifficulties who may require a more comprehensive assessment or professional management. Itconsists of 175 items that asses the following scales: reliability and validity; basic personalityaspects, pathological personality, moderate clinical syndromes and severe clinical syndromes.Easy to use, the interpretative procedures are computerised and the user can obtain them on thespot in the case of outpatients in mental health centres, general hospitals or private clinics for anexpert report. There are cut-off points in the scales to aid decision-making when faced withbehavioural disorders or clinical syndromes. Its application can be individual and collective,with completion time ranging from 20 to 25 minutes (individuals 18 years and older) 377 .Spanish version of the MCMI-IIIThere is a version adapted by TEA publishing house 378MACI (adolescent version of the MCMI-III)The MACI (Millon Adolescent Clinical Inventory) has been designed to assess personalitycharacteristics and clinical syndromes in adolescents aged 13-19 years. It is applied on anindividual basis. Its specific design for adolescents contrasts with other questionnaires aimed atthe adult population. The whole theoretical system it is based on and the confluence ofdiagnostic suggestions and elements shared with the current DSM-IV, as well as a completevalidation study, make it a valuable and relevant instrument. It is especially useful for theCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS182

assessment and confirmation of diagnostic hypotheses, for treatment planning and for measuringprogress in the different phases of treatment. It is comprised of 160 items that are grouped in 27scales that encompass three main dimensions: personality characteristics, expressed concernsand clinical syndromes. Cut-off points are provided to aid decision-making in the case ofdisorders or clinical syndromes and validity and control indexes (original version of the MACI).Spanish version of the MACIThere is a version adapted by TEA publishing house 379TCI-RRevised version of the Temperament and Character Inventory. Cloninger,et al., 1994The TCI-R is a self-report instrument that quantifies seven personality dimensions and 25secondary traits. It contains 240 items on a 5-point Likert scale. This questionnaire has beenused in students, general population and clinical population. Its psychometric properties, as wellas the empirical work conducted with the TCI-R, are described in the development group’smanual 380 .Spanish version of the TCI-RThere is a version that has been adapted and validated in our setting by JA Gutiérrez-Zotes, etal., 2004, in a sample of 400 volunteers (18-65 years) from geographic areas of Madrid,Tarragona and Barcelona 381 . This group had already developed the Spanish version of theoriginal TCI 382 .IPDEInternational Personality Disorder Examination. Loranger, 1979The IPDE is a diagnostic tool, based on a semistructured clinical interview that is compatiblewith ICD-10 and DSM-IV assessment criteria. Its results enable the measure of other majorpersonality disorder categories that until now had been omitted, providing a uniform reliablediagnosis that can be internationally accepted 383 .Spanish version of the IPDEThere is a Spanish version that was developed by López-Ibor, et al., 1996 38410.2.5. ObsessivenessY-BOCSYale-Brown Obsessive-Compulsive Scale. Goodman et al., 1989In 1989 Goodman, et al. designed the Y-BOCS scale for OCD defined in terms of DSM-III-Rcriteria. The scale measures the intensity of OCD without analysing symptom content; it assessesobsessions and compulsions separately; it is sensitive and selective in changes of symptomseverity. It is not a diagnostic tool, it is quickly and easily applied, and does not confound traitand state variables. Hence, the Y-BOCS has been designed to be used in patients with an OCDdiagnosis, constituting an adequate method to measure severity of symptoms and their variationdue to treatment. Several comparison and validation studies have been conducted to compareinstruments designed to measure obsessive-compulsive symptomatology and Y-BOCS standsCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS183

out as the most adequate, given its higher reliability, internal consistency and sensitivity tochange 385 .Spanish version of the Y-BOCSThere is a version adapted and validated in our setting by Sal, et al., 2002 386CY-BOCS (children and adolescent version of the Y-BOCS)Spanish version of the CY-BOCSThere is a version that has been adapted and validated in our setting by Ulloa, et al., 2004 387Recommendation 10.2. It is recommended to use questionnaires that have been adapted andvalidated in the Spanish population for the psychopathological assessmentof eating disorders. At present, the following instruments arerecommended to carry out the psychopathological assessment of eatingdisorders (version selection based on age and other applicationconditions):- Impulsiveness: BIS-11- Anxiety: STAI, HARS, CETA- Depression: BDI, HAM-D, CDI- Personality: MCMI-III, MACI, TCI-R, IPDE- Obsessive ness: Y-BOCS.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS184

11. Prognosis of Eating DisordersKey Questions:11.1. What is the prognosis of eating disorders?11.2. Are there prognostic factors for eating disorders?11.1. What is the prognosis of eating disorders?Anorexia nervosaThere are contradictory data on the prognosis of AN despite its long historical trajectory,motivated by several factors: follow-up studies with great temporal variability, different resultsdepending on when these studies are performed, lack of randomised intervention studies withsufficient outcome assessment, etc.Acknowledging the previous limitations, results derived from the review of the mainstudies and SRSE of AN prognosis indicate that: mean gross mortality rate is 5% with a highstandard deviation (5.7) and a 0 to 22 interval 388, 389 . Gross mortality rates are generally superior tothose of the general population and increase significantly with the duration of follow-up. Incontrast to this data, it seems that the overall outcome in survivors improves with duration offollow-up (with the resulting therapeutic implications).50% of AN cases resolve in complete remission 390-392 . Partial remission is observed in 20%-30% of AN cases 388, 391 . Between 10% and 20% of cases result in chronicity 389, 391, 393 .Bulimia nervosaThe natural course of BN at 5 years in patients who live in a community is as follows: eachyear, 33% result in remission and 33% in relapse. This information indicates a relatively poorprognosis for non-treated individuals 74 .In 6-year follow-up studies of treated individuals, 60% were determined to have goodprognosis, 30% were considered partially recovered and 10% were determined to have poorprognosis 394 .Risk factors of diagnosis modification (AN to BN or vice versa)There is a lack of prospective studies focused on the evolution of AN based on the survivalanalysis model. However, the following risk factors for diagnosis modification from AN to BNor from BN to AN are: low self-sufficiency or autonomy, high paternal criticism, alcohol185CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

abuse/dependency, low sensation seeking level 395 .Binge-Eating DisorderIn follow-up studies at 5 years, 10% of cases diagnosed with BED maintained the diagnosis,18% to 20% presented partial remission and 70% were determined to have good prognosis. Thepresence of binge-eating predicts weight gain. The prevalence of obesity was duplicated in thegroup of patients who presented disorder maintenance by the end of the study 74 .11.2. Are there prognostic factors in eating disorders?Anorexia nervosa– Good prognostic factors: histrionic personality traits 388 , onset in adolescence 393, 396 . In thelatter case, it would not exactly be a good prognostic factor but rather a better prognosticfactor than onset of AN in adulthood.– Poor prognostic factors: comorbidity with other psychiatric disorders (mood disorders,anxiety disorders, substance abuse), presence of self-induced vomiting, binge-eating orlaxative abuse, obsessive-compulsive personality traits, social adjustment and diseaseduration 388, 395, 397 .Bulimia nervosa– Good prognostic factors: the earlier treatment has been initiated, the better prognosis.This factor is deemed to be the best indicator of good prognosis, even more than the type orduration of given treatment 398 ; it also correlates with good prognosis at the beginning of thedisease in adolescence when compared to onset in adulthood 399 .– Poor prognostic factors: history of substance abuse or laxative abuse predict suicideattempts 400 ; comorbidity with OCD is associated with longer disease duration 401 ; history ofeating conflicts and/or refusal at early stages of childhood 402 ; poor psychosocial functioningand greater disturbance of body image are the factors that most influence BN relapse 403 .Binge-Eating Disorder– Poor prognostic factors: the presence of binge-eating episodes predicts weight gain. Theprevalence of obesity was duplicated in the group of patients who sustained BED by theend of the study 74 . The presence of Cluster B personality traits predicts greater frequency ofbinge-eating episodes 404 .CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS186

12. Legal Aspects Concerning Patientswith Eating Disorders in SpainKey Questions:12.1. What legal procedure must be followed when a patient with an eatingdisorder refuses to receive treatment?12.2. Is the informed consent of a minor with an eating disorder legally valid?12.3. In the case of a minor with an eating disorder, what is the legal solution to thedilemma stemming from the responsibility of confidentiality, respect ofautonomy and obligations towards the minor’s parents or legal guardians?12.1. What legal procedure must be followed when apatient with an eating disorder refuses to receivetreatment?To receive a medical treatment an informed consent is needed after the patient is informedof all the pertaining information in relation to the treatment, in virtue of Article 10 of the EthicsCode 405 and Articles 4, 8 and 9 of Law 41/2002 406 .Legally, the informed consent form is a non-transferable, non-delegable personal act. It isnot a formal legal act and because of this it is not regulated by the civil code. Hence, thepersonal informed consent of the patients is a right that must be respected at all times, save forthose exceptions explicitly established by the law.One exception to the above is the lack of capacity of the patient. Spanish law allows thephysician to carry out any clinical interventions that are essential even without the consent of theaffected individual (article 9.2 Law 41/2002) 406 in cases where there is severe immediate risk tothe individual’s physical or mental integrity, prior consultation with family members or peoplerelated to the affected individual.The application of Law 41/2002 406 sets forth some exceptional scenarios to the valid consentof a patient aged 16-17 years, since the legal age to make health-related decisions is 16 years inthe application scope of this guide.Any treatment that might require admission to hospital (article 9.4 Ethics Code) 405 must beregulated by the organic law and provide sufficient warranties, as it represents an exception to187CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

the freedom of articles 17 of the Spanish Constitution 407 and 5 of the Rome Convention of the 4 thof November, for the protection of human rights and fundamental freedoms 408 .In cases where total hospitalisation is deemed essential without having obtained theinformed consent, article 763 of Law 1/2000 of 7th of January of the Civil Procedures Rules 409establishes the occurrence of two situations: for the condition to be a psychological/psychiatricdisorder and for the affected individual to be unable to make his or her own decisions.Two situations are foreseen:a) To apply for a Court authorisation for voluntary admission to hospital.b) To admit the patient first and to report the admission to the Court with jurisdiction overthe case within 24 hours.In either of these two scenarios, it is a non-contradictory procedure before a Court, beingthe affected individual able to express his or her agreement or disagreement by themselves and ifthe individual so requires by means of representation and defence. The Court will issue either anorder of authorisation or denial that will be open to appeal. The Court will state in the order theobligation on the part of the physicians to inform such Court of the need to maintain the measureevery six months, being possible to establish a shorter period depending upon the type ofdisorder.It is the physician’s ultimate responsibility to decide when to discharge the hospitalisedindividual and the physician shall inform the Court immediately of such decision.RecommendationAccording to current legislation12.1 The use of legal (judicial) channels is recommended in caseswhere the health professional deems it appropriate to safeguardthe health of the patient, observing in all circumstances thepatient’s right to be heard and to be conveniently informed of theprocess and the medical and legal measures that will be applied.The well-informed procedure not only respects the right toinformation but also encourages the patient’s cooperation andmotivation and that of his or her closer relatives in the totalhospitalisation procedure.188CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Current legislation– Article 10 of the Ethics Code and Medical Deontology, 1999. OMC, Revista delConsejo General de Colegios Médicos de España, 1999 (66): 2.124 y 2.931 405 .– Articles 4, 8 and 9 of Law 41/2002, of 14th November, a basic regulatory law that governs thepatient’s autonomy and embraces rights and obligations concerning clinical information anddocumentation (State’s Official Gazette no. 274, dated 15-11-2002, pp. 40.126-40.132) 406 .– Article 9.2 of Law 41/2002, of 14th November, a basic regulatory law that governs thepatient’s autonomy and embraces rights and obligations concerning clinical information anddocumentation (State’s Official Gazette no. 274, dated 15-11-2002, pp. 40.126-40.132) 406 .– Article 9.4 of the Ethics Code and Medical Deontology, 1999. OMC, Revista del ConsejoGeneral de Colegios Médicos de España, 1999 (66): 2.124 y 2.931, concerning observance ofthe patient’s freedom and the possibility to request judicial intervention, if and whennecessary 405 .– Article 17.1 of the Spanish Constitution of 6th of December 1978, concerning the right tofreedom and the prohibition against deprivation of freedom, save for those cases expresslystipulated by the Law, as approved by the General Courts in plenary sessions of the Congressof Deputies and the Senate held on the 31 st of October 1978 and ratified by the Spanishpeople via referendum on the 6th of December 1978 and sanctioned by his Royal Majesty theKing before the General Courts on the 27 th of December 1978 407 .– Article 5 of the European Convention for the Protection of Human Rights and FundamentalFreedoms of 4 th November, ratified by Spain with date 26 th of September 1979 and publishedin the Spanish Official Gazette on the 10 th of October 1979. Revised in conformity withProtocol number 11 (coming into effect date 1 November 1998), based upon which thecauses for non-voluntary admission to hospital may only be regulated by law 408 .– Article 763 of Law 1/2000, of 7th of January of the Civil Procedures Rules. Non-voluntaryadmission to hospital due to a psychological/psychiatric disorder, which regulates two types:non-voluntary admission to hospital and emergency admission to hospital 409 .CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS189

12.2. Is the informed consent of an under-age individualsuffering from ED legally valid?Legislation accepts the legal validity of the minor’s autonomy contingent upon the minor’slevel of maturity in accordance with Organic Law for the Protection of Minors 1/1996, of 15 th ofJanuary, which regards the minor as a titleholder of rights and not just as a mere object of suchrights 410 .The legal treatment (article 9.3.c. of Law 41/2002) of an informed consent issued by aminor takes into account objective considerations (age) as well as subjective considerations (thepatient’s capacity to discern correctly) 406 .In general, in lieu of the Spanish legislation, the physician is obliged to listen to the minor(article 10.6 of the Ethics Code 405 and article 9.3.c. of Law 41/2002 406 ) and make the will of thefamily prevail in those cases in which the minor is unable to decide neither emotionally norintellectually, by means of the informed consent form, under the following legal limitations:• It is the obligation of the physician to always listen to minors aged 12 and over and to takeinto account their opinion contingent upon their level of mental growth and personalattitude, making them participate in as much as possible in the making of decisionsthroughout the health process.• Over the age of 16, the Law understand that the consent must be rendered directly by thepatients in all cases, save for situations that pose severe immediate risk to health, in whichthe physician shall only inform and listen to the parent’s views and opinions.RecommendationAccording to current legislation12.2 One characteristic symptom of EDs and specifically of AN is theabsence of awareness of the disease among sufferers. The diseaseitself often causes a lack of sufficient judgement to issue a valid andunbiased consent concerning the acceptance and choice oftreatment. Hence, in the assumptions of severe risk to the health of aminor afflicted with AN who refuses treatment, established legaland judicial channels must specially be followed.190CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Current legislation– Organic Law 1/1996, of 15th of January, for Legal Protection of Minors, partial amendmentof the Civil Code and the Civil Procedures Rules Law. Spanish Official Gazette, 17 th January1996 (number 0015) 410 .– Article 9.3.c. of Law 41/2002, of 14th November, a basic regulatory law governing thepatient’s autonomy and the rights and obligations with regard to clinical information anddocumentation (Official Gazette no. 274, de 15-11-2002, pp. 40.126-40.132) 406 .– Article 10.6 of the Ethics Code and Medical Deontology, 1999. OMC, Revista del ConsejoGeneral de Colegios Médicos de España, 1999 (66): 2.124 y 2.931, concerning observanceof the patient’s freedom and possibility to apply for the intervention of the Court, in caseswhere deemed necessary 405 .12.3. In the case of a minor diagnosed with ED, how is thedilemma: duty of confidentiality, respect to autonomy,and obligations with regard to the parents or legalguardians of the minor solved?The controversy between the knowledge and authorisation from the parents or legalguardians and the right to privacy and confidentiality of the minor (article 7 of Law 41/2002) 406 ,is present in all norms and regulations and there is not one single norm that serves as a guide tothe physician to generalise cases. In general, regulation tends to be inspired on some generalprinciples concerning respect to privacy and professional secret, and to establish certainlimitations and exceptions to the main general principle.The physician may –according to article 16.1.d) of the Ethics Code 405 – disclose the secretprior authorisation from the patient or without such authorisation in cases in which thephysician’s silence may cause damage to the actual patient or to third parties.Likewise, in an extended reading of the Civil Code on how the minor must be regarded, it isimportant for the physician to take into account the minor’s age and maturity level.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS191

RecommendationAccording to current legislation12.3 The balance among the different rights in conflict makes it mandatory forthe physician to observe and to interpret the best solution to each case.Nonetheless, it is always of outmost importance to inform and to listenattentively to both sides so that they understand the relationship betweensafeguarding health and the decision taken by the physician.Current legislation– Article 7 of Law 41/2002, of 14th November, a basic regulatory law governing the patient’sautonomy and the rights and obligations with regard to clinical information anddocumentation (Official Gazette no. 274, de 15-11-2002, pp. 40.126-40.132) 406 .– Article 16 of the Ethics Code and Medical Deontology, 1999. OMC, Revista del ConsejoGeneral de Colegios Médicos de España, 1999 (66): 2.124 y 2.931, concerning exceptionsto the physician’s professional secret 405 .– Law 41/2002, of Law 41/2002, of 14th November, a basic regulatory law that governs thepatient’s autonomy and embraces rights and obligations concerning clinical information anddocumentation (State’s Official Gazette no. 274, dated 15-11-2002, pp. 40.126-40.132) 406 .– Instrument of ratification for the Convention for the Protection of Human Rights and theDignity of Human Beings, with regard to the applications of biology and medicine(Convention relating to Human Rights and Biomedicine) signed in Oviedo on the 4 th ofApril 1997. Official Gazette number 251 of 20th October 1999 411 .– European Convention for the Protection of Human Rights and Fundamental Freedoms of 4 thNovember, ratified by Spain with date 26 th of September 1979 and published in the SpanishOfficial Gazette on the 10 th of October 1979. Revised in conformity with Protocol number 11(coming into effect date 1 November 1998) 408 .– Law 1/2000, of 7th of January, of Civil Procedures Rules (Official Gazette. 7, of 8th January2000, pp. 575-728. Error corrections that appeared in the Official Gazette no. 90, de 14-04-2000, p. 15.278 and Official Gazette no. 180, dated 28-07-2001, p. 27.746) 409 .– Order 129/99 issued by the Constitutional Court concerning circumstances for nonvoluntaryadmission to hospital. 412CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS192

13. Detection, diagnosis and treatmentstrategies for eating disordersCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS 193

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Algorithm NotesAlgorithm 1. Detection of potential cases of eating disorders1) Visits of healthy children/adolescents and visits prior to participating in sports, for example,would be a good opportunity to carry out integrated prevention (primary) and screening ofdifferent disorders, including eating disorders.2) Screening instruments are useful for a quick, first assessment aimed at ruling out theexistence of suspicious symptoms in the first phase of the two-phase screening process, inwhich individuals who obtain high scores are re-assessed to determine if they fulfil formaldiagnostic criteria.3) Screening instruments are inefficient at establishing the diagnosis of an eating disorder.4) In order to identify potential cases of eating disorders, several different screening selfreportedquestionnaires have been designed that enable systematic assessment of eatingbehaviour.5) It is recommended to use questionnaires that have been adapted and validated in the pulationto detect cases (screening) of eating disorders. The following instruments are recommended(Good clinical practice). Recommendation 6.5.:– Eating disorders in general: SCOFF (for individuals aged 11 years and over).– AN: EAT-40, EAT-26 and ChEAT (the latter for individuals aged between 8 and 12years).– BN: BULIT, BULIT-R y BITE (the three for individuals aged 12-13 years and over).Algorithm 1 abbreviationsPC = Primary CareBITE = Bulimic Investigatory Test, EdinburghBULIT = Bulimia TestBULIT-R = revised version of the BULITChEAT = Children’s version of the EAT-26EAT-40 = Eating Attitudes TestEAT-26 = Abbreviated version of the EAT-40SCOFF = Sick, Control, One, Fat, Food questionnaireEDs = Eating DisordersCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS197

Algorithm 2. Intervention if there is suspicion of an eating disorder1) If a person attends the primary care practice presenting symptoms of a suspected eatingdisorder, the clinician must assess whether he/she is in a borderline biological or mentalsituation after performing basic examinations and blood work.2) If the person seeking help is aware of the problem, the standard diagnostic proceduremust be carried out, including anamnesis, physical and psychopathological examinationsand complementary examinations (Good clinical practice). Recommendation 7.2.4.3) Although communication must always be established with the family, the health carepractitioner must study the patient’s family environment and generate a climate of trustand confidentiality. When it is the family that seeks help, it becomes a key piece in thephysician-patient relationship.4) It is recommended to follow the WHO’s (ICD-10) and the APA’s (DSM-IV or DSM-IV-TR) diagnostic criteria. (Good clinical practice). Recommendation 7.1.5) NC is provided with the aim of modifying what the patient eats, as well as maladaptiveeating habits and attitudes. The advice given includes the description of a healthy diet,the benefits of maintaining a regular eating schedule, eating three meals a day, eatingnormal rations according to age, eating with the family, in a relaxed environment withoutdistractions, without being the one to prepare the meal or staying in the kitchen andresting after meals, amongst others. Weight restoration requires a normocaloric andhealthy diet except in cases where it is contraindicated due to the patient’s condition.6) Criteria for referral from PC to the hospital (emergency service of a general hospital)depend on whether the emergency is medical or psychiatric.Criteria for referral from PC to emergency hospitalisation (emergency service of a generalhospital) to receive emergency medical treatment are as follows:– Weigh loss >50% in the last 6 months (30% in the last 3 months)– Consciousness disturbances– Convulsions– Dehydration– Severe liver or kidney disturbances– Pancreatitis– Decreased potassium

Criteria for referral from PC to emergency psychiatric assessment (psychiatric service of ahospital) are as follows:– Absolute refusal to eat or drink.– Depressive symptomatology, with autolytic risk.– Significant self-inflicted injury behaviour.7) Criteria for referral from PC to adult or child/adolescent mental health centres/units are asfollows:– When there is an established diagnosis of eating disorder.– Weight loss equal to or higher than 10%-25% of weight, without a justifiable cause.– Presence of regular bulimic episodes, meaning binge-eating behaviour and/or persistentpurging practices (self-induced vomiting, laxative abuse and use of diuretics).– Presence of associated psychopathological disturbances.– Lack of disease awareness.– If neither weight nor bulimic behaviour improve after following PC guidelines.8) Complete hospitalisation (inpatient care) criteria:– The biological state entails serious risk of complications (no consumption of food orliquids, BMI

9) Day care admission criteria:– From the adult or children’s mental health centre. If the patient does not meet emergencymedical care or emergency inpatient treatment in a psychiatric hospital criteria and does fulfilone of the following criteria:– The patient is unable due to her psychopathological state to follow the guidelines of theoutpatient treatment programme: frequency of visits, limitation of physical activity,recommended diet, etc.– There are serious behavioural problems in the patient’s home, family conflicts and/orfamily psychopathology that are not modified on an outpatient basis.– Weight progress does not follow the rate established in the outpatient weight restorationprogramme.– From inpatient care (complete hospitalisation) (once discharge criteria have been fulfilled).More control must be exercised on eating and diet and disordered behaviour and though it canalso be performed on an outpatient basis, it is not indicated if there are serious behaviouralproblems in the patient’s home, family conflicts and/or history of family psychopathology thatcannot be modified by outpatient management.Algorithm 2 abbreviationsPC = Primary careMHC = Mental health centreNC=Nutritional counsellingDH = Day hospitalNC = Nutrional counsellingEDs = Eatind DisordersCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS200

Algorithm 3. Treatment of AN1) It is recommended to follow the WHO’s (ICD-10) and the APA’s (DSM-IV or DSM-IV-TR) diagnostic criteria to establish the diagnosis of AN. (Good clinical practice).Recommendation 7.1.2) Nutritional or dietary counselling. This type of intervention aims mainly to modify whatthe patient eats, as well as maladaptive eating habits and attitudes, providing a model tofollow (description of a healthy diet, the benefits of maintaining a regular eating schedule,eating three meals a day, eating normal rations according to age, eating with the family, ina relaxed environment without distractions, without being the one to prepare the meal orand resting after meals, amongst others.). A normocaloric and healthy diet is required forweight restoration, except in cases where it is contraindicated due to the patient’s condition.– In feeding guidelines for children and adolescents with anorexia nervosa, carers should beincluded in any dietary information, education and meal planning. (Grade D).Recommendation 9.GM.1.3) Renutrition– Performance of standard treatments to resolve the situation acknowledging individualneeds, especially in the case of children and adolescents. (Grade D). Recommendation9.GM.1.– A physical exploration and in some cases oral multivitamin and/or mineral supplements arerecommended, both in outpatient and inpatient care, for patients with AN who are in thestage of body weight restoration. (Grade D). Recommendation 9.1.1.1.– Feeding against the will of the patient should be used as a last resort in the management ofAN. It is an intervention that must be performed by experts in the management of eatingdisorders and related clinical complications. Legal requirements must be taken into accountand complied with when deciding whether to feed a patient against his/her will. (Grade D).Recommendations 9.GM.2, 9.GM.3 and 9.GM.4.Total parenteral nutrition should not be used in patients with AN unless the patient refusesnasogastric feeding and/or when there is gastrointestinal dysfunction. (Grade D).Recommendation 9.1.1.2.– Nutritional support for patients with eating disorders will be selected based on the patient’sdegree of malnutrition and collaboration, and always with the psychiatrist’s approval.(Good clinical practice). Recommendation 9.GM.01.– Before initiating artificial nutrition the patient’s degree of collaboration must be assessedand an attempt must always be made to convince him/her of the benefits of natural feeding.(Good clinical practice). Recommendation 9.GM.02.– In day hospitals, nutritional support for low-weight patients, where an oral diet isinsufficient, can be supplemented with artificial nutrition (oral enteral nutrition). To ensureits intake, it must be administered during the day hospital’s hours, providing supplementaryenergy ranging from 300 to 1,000 kcal/day. (Good clinical practice). Recommendation9.GM.03.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS201

– Oral nutritional support in eating disorder inpatients is deemed adequate (favourableprogress) when a ponderal gain greater than 0.5 kg per week is produced, with up to 1 kgincrements being the usual during that period. Sometimes, when the patient withmoderate malnutrition resists resuming normal feeding, the diet can be reduced by 500-700 kcal and be supplemented by complementary oral enteral nutrition in the sameamount, which must be administered after meals and not instead of meals (Goodclinical practice). Recommendation 9.GM.04.– In the case of severe malnutrition, extreme starvation, poor progress or lack ofcooperation of the patient in terms of eating, artificial nutrition treatment is indicated. Ifpossible, an oral diet with or without oral enteral nutrition is always the first step,followed by a 3 to 6 day period to assess the degree of collaboration and medicalnutritionalevolution. (Good clinical practice). Recommendation 9.GM.05.– Regarding estimated energetic requirements, it is recommended that caloric needs at thebeginning always be below the usual, that real weight, as opposed to ideal weight, is usedto make the estimation and that in cases of severe malnutrition energetic requirements be25 to 30 kcal/kg real weight or total kcal not higher than 1,000/day. (Good clinicalpractice). Recommendation 9.GM.06.4) Pharmacological interventions– Pharmacological treatment is not recommended as the only primary treatment of AN.(Grade D). Recommendation 9.GPH.1.– Caution should be exercised when prescribing pharmacological treatment for patientswith AN who have associated comorbidities such as obsessive-compulsive disorder(OCD) or depression. (Grade D). Recommendation 9.GPH.2.– If drugs with adverse cardiovascular effects are administered, ECG monitoring of patientsshould be carried out. All patients with AN must be warned of the side effects ofpharmacological treatments. (Grade D). Recommendations 9.GPH.4 and 9. GPH.5.5) Psychological therapiesThe objective of psychological treatment is to reduce risk, to encourage weight gain by means ofa healthy diet, to reduce other symptoms related with eating disorders and to facilitate physicaland psychological recovery. (Grade D). Recommendation 9.GP.3.The psychological therapies that should be considered for AN are: CBT, SFT, IPT, PDT and BT.(Grade D). Recommendation 9.GP.1.– The duration of psychological treatment should be of at least 6 months when performedon an outpatient basis (with physical monitoring) and 12 months for individuals who havebeen under inpatient management. (Grade D). Recommendation 9.GP.5.– For patients with AN who have undergone outpatient psychological therapy but have notimproved or have deteriorated, the indication of more intensive treatments (combinedindividual and family therapy, day or inpatient care) must be considered. (Grade D).Recommendation 9.GP.6.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS202

– Following hospital discharge, patients with AN should be offered outpatient care thatincludes monitoring of normal weight restoration and psychological intervention thatfocuses on eating behaviour, attitudes to weight and shape and the fear of social responseregarding weight gain, along with regular physical and psychological follow-up. Follow-upduration must be of at least 12 months. (Grade D). Recommendation 9.GP.10.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS203

Algorithm 4. Treatment of BN and BED1) It is recommended to follow the WHO’s (ICD-10) and the APA’s (DSM-IV or DSM-IV-TR) diagnostic criteria to establish the diagnosis of BN and BED. (Good clinicalpractice). Recommendation 7.1.2) Nutritional counselling and dental hygiene adviceThis type of intervention aims mainly to modify what the patient eats, as well as maladaptiveeating habits and attitudes, providing a model to follow (healthy diet, maintenance of a fixedeating schedule, eating three meals a day, eating normal rations according to age, eating with thefamily in a relaxed environment without distractions, without being the one to prepare the mealand resting after eating).In the case of laxative misuse, patients with BN must be advised on how to decrease and stopabuse. This process must be carried out gradually. Patients must also be informed that the useof laxatives does not decrease nutrient absorption. (Grade D). Recommendation 9.GM.8.When electrolyte imbalance is detected, in most cases elimination of the behaviour that caused itis sufficient to correct the problem. In a small number of cases, oral administration ofelectrolytes whose plasmatic levels are insufficient is necessary to restore normal levels, exceptin cases involving gastrointestinal absorption. (Grade D). Recommendation 9.GM.7.Patients who vomit habitually must have regular dental check-ups and be provided with dentalhygiene advice. (Grade D). Recommendation 9.GM.9.3) Psychological therapies– CBT-BN is a specifically adapted form of CBT and it is recommended that 16 to 20 sessionsare performed over 4 or 5 months of treatment. (Grade A). Recommendation 9.3.2.1.1.Patients with BN who do not respond to or refuse to receive CBT treatment may be offeredalternative psychological treatment. (Grade B). Recommendation 9.3.2.1.2.Adolescents with BN can be treated with CBT adapted to their age, level of development, and, ifappropriate, the family’s intervention can be incorporated. (Grade D). Recommendation9.3.2.1.3.Adult patients with BED can be offered a specifically adapted form of CBT. (Grade A).Recommendation 9.3.3.1.– A possible first step in the treatment of BED is to encourage patients to follow a SHprogramme (guided or not). (Grade B). Recommendation 9.GP.13.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS204

Health care professionals can consider providing BED patients with SH programmes (guided ornot) that may yield positive results. However, this treatment is only effective in a limitednumber of patients with BED (Grade B). Recommendation 9.GP.14.– If there is a lack of evidence to guide the care of patients with EDNOS or BED, health careprofessionals are recommended to follow the eating disorder treatment that most resemblesthe eating disorder the patient presents. (Grade D). Recommendation 9.GP.15.– IPT should be considered an alternative to CBT although patients should be informed that itrequires 8 to 12 months to achieve results similar to those obtained with CBT. (Grade B).Recommendation 9.5.2.1.IPT-BED can be offered to patients with persistent BED. (Grade B). Recommendation9.5.3.1.4) Pharmacological interventions– In the treatment of BN pharmacological treatments other than antidepressants are notrecommended (Grade B). Recommendation 9.9.2.1.2.Patients should be informed that antidepressant treatment can reduce the frequency of bingeeatingand purging but effects are not immediate. (Grade B) Recommendation 9.9.2.1.1.The dose of fluoxetine used in patients with BN is greater than the dose used for treatingdepression (60 mg/day). (Grade D). Recommendation 9.9.2.1.3.Amongst SSRI antidepressants, fluoxetine is the first-choice drug for treatment of BN, in termsof acceptability, tolerability and symptom reduction. (Grade D). Recommendation 9.9.2.1.4.– SSRI antidepressant treatment can be offered to a patient with BED, regardless of whetherhe/she follows a guided SH programme or not. (Grade B). Recommendation 9.9.3.1.1.Patients must be informed that SSRI antidepressant treatment can reduce the frequency of bingeeating,but the duration of long-term effects is unknown. Antidepressant treatment may bebeneficial for a small number of patients. (Grade B). Recommendation 9.9.3.1.2.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS205

14.Dissemination and implementationIn order for this CPG to reach health care professionals in the NHS, its dissemination willbe carried out by means of the GuíaSalud Catalogue (www.guiasalud.es) and CAHTA’s website(www.aatrm.net).Once the national dissemination Plan within the general framework of GuíaSalud has beencompleted, the guide’s working group and CAHTA will perform further dissemination activitiesthat are deemed appropriate.The CPG consists of three versions for health care professionals: the full version, thesummary and the quick version. The first two include information for patients (Annex 3). TheCPG is edited electronically and is available on the GuíaSalud and CAHTA websites. Thesummarised and quick versions are also in book and leaflet form, respectively. The bookcontains the CD-ROM of all versions.The measure of adherence or implementation of the CPG’s recommendations by means ofmonitoring and/or auditing can improve its use. The manual of the AGREE instrumentaddresses the importance of elaborating indicators, item 21 of the “applicability” dimensiontackling this issue 45 . Hence, a CPG must offer a list of clear quantifiable criteria or qualityindicators that derive from the key recommendations in the guide. The most well known andwidely used indicator classification system in this guide is the one pertaining to Donabedian 413 ,which classifies indicators into: structure, process and outcome. In order to determine and assessthe performance of the most important recommendations, the assessment of certain interveningprocess variables and the most relevant clinical outcomes is suggested.In the clinical assessment of eating disorders it is recommended to measure key aspectsrelated with quality for which certain indicators are initially proposed due to their validity,reliability and feasibility at different levels of care (primary care and specialised care).Table 1 describes the 11 proposed indicators according to clinical area, type of indicator,the dimension of quality they address and the care level where they may be applied. It isimportant to borne in mind that, in practice, available indicators are not perfect and constitute anapproximation of a real situation. Their objective is to provide useful information to facilitatedecision-making. They are quantitative measures, which, if obtained periodically, enableanalysis of their evolution over time (monitoring) 1 .Some of the indicators included in the Mental Health Strategy of the NHS (Quality Plan) 414are common to eating disorders. Therefore, some of the indicators proposed are common tothose included in the above-mentioned plan. Others have been adopted from the ContractProgramme of the Regional Ministry of Andalusia/Andalusian Health Service 415 and the NICECPG 30 . Additionally, the working group has proposed others.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS206

Table 1. Proposed indicatorsAreaType ofindicatorName of the indicator(standard)QualitydimensionHealth carelevelsusceptible toapplication1 2 3Referral Process Proportion of patients with eating disorderswho have been adequately referred to aspecialised care level (See Annex 2.10.)AdequacyxReferral Process Proportion of patients with eatingdisorders who have been adequatelyreferred with emergency criteria (SeeAnnex 2.10.)Adequacy x xReferral Process Average time elapsed between hospitaldischarge and the first outpatient (adult orchildren MHC) or day care follow-up visit(standard 70%)Adherence totreatmentx x xFollow-up Process Proportion of patients diagnosed with aneating disorder during outpatient monitoringin day care or in the adult or children MHCwho are discharged based on the number ofmonths of follow-up (standard >60%)Effectiveness/ResolutionxxFollow-up Process Number of interviews with familymembers in relation to visits for patientsdiagnosed with an eating disorder(standard 1/month)Integralcarex x xFollow-up Outcome Percentage of readmissions to thegeneral hospital at 3, 6, 9 and 12months.(See Annex 2.10.)Effectiveness/Continuity ofcarexxDiagnosis Outcome Proportion of patients seen with an eatingdisorder diagnosis in PC, adult or childrenMHC, day hospital and general hospital.(see Annex 2.10.)Diseasemanagementx x xCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS207

IntegralcareOutcomeSatisfaction index of patients andfamily members by the end oftreatment (see Annex 2.10.)Satisfaction x x xIntegralcareOutcome Number of complaints (standard

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15. Future research recommendationsThe following studies are required:Studies that clarify the benefits, versus potential risks, of primary prevention programmes inschools and in mass media.Studies that describe the value of preventive interventions (screening and risk factors) in childhoodand adolescence, considered the highest risk group for developing eating disorders.Studies that improve evidence regarding the choice of the treatment prescribed, the selection ofother specific instruments and the expected duration and intensity of treatment in order toachieve the best results (immediate and long-term), based on clearly defined clinical indicatorsand on a more precise description of the stages of these disorders.Studies that determine predisposing and precipitating biological and genetic risk factors foreating disorders. Also determine environmental, neuropsychological and personality risk factorsthat serve as precursors-protectors of eating disorders.Studies that address proper methods for the treatment of osteopenia, osteoporosis and other“diseases-sequelae” of AN.In the case of AN, studies that assess specific treatments for your patients, who are probablymore sensitive to treatment and should be differentiated from treatments designed for olderpatients and patients with more chronic diseases, since that the characteristics and response totreatment, in other diseases, varies between these groups. Large multi-centre studies withadequate strength and required given that it is hard to recruit and retain patients with AN incontrolled treatment studies due to the high dropout rate.In the case of BN, studies that help to determine predictive factors of therapeutic success-failureand early predictors of change. Better studies are also required to address the treatment ofcomplex cases with multiple comorbidities that are so common in health care practice.In the case of BED, combined with obesity, studies on the best sequence of treatments (forexample, if BED treatment precedes, or not, weight management treatment) and on the longtermbenefits of treatment in terms of eating disorder symptoms and weight.Studies that analyse in depth the clinical-phenomenological intrinsic characteristics ofEDNOS (clinical and personality) and the efficacy of specific therapeutic approaches.Studies that analyse the clinical-phenomenological characteristics of less prevalent eatingdisorder groups (late onset, males, etc.) and the efficacy of specific treatments.Studies on the development and validation of SH therapeutic programmes not only in a printedformat, but also and especially using the latest technological instruments (computerisedCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS210

manuals) and remote help (online, telephone support, etc.).Studies that analyse endophenotypes associated with eating disorders (purging cases, impulsivesubgroups, etc.) and therapeutic efficacy.Studies that analyse cognitive styles and neuropsychological processes involved in the onset andmaintenance of eating disorders.Studies that analyse the clinical impact of comorbidity (Axis I and II) on eating disorders andspecific therapeutic efficacy. Additionally, it would be necessary to design and analyse specifictherapeutic approaches in these patient groups.Studies that provide an in-depth analysis of diagnosis modification and factors involved ineating disorders.Studies on the efficacy-efficiency of health care resources: structural and managementaspects.Studies that provide an in-depth analysis of the utility of new technologies (telemedicine,Internet, short mobile text messages [sms], videogames), as an additional therapeutic tool and inspecialist education and training procedures.Studies on neuroimaging, to facilitate an understanding of the morphological and functionalinvolvement of certain brain areas in eating disorders (biological, environmental and personalityvulnerability, nutritional changes associated with eating disorders, areas that regulate fullnesshungersensations and therapeutic efficacy).Animal and human studies on the mechanisms that regulate eating, versus energy expenditure.Studies on the links between physiological and psychological processes of puberty and the onsetof eating disorders.Studies on the effects of exercise, including the role of extreme exercise and eating restraint, onthe onset and development of eating disorders; and the opposite, the possible protective effect ofsome healthy popular athletes on boys’ and girls’ attitudes towards exercise, diet, weight andshape.Studies on the impact of several comorbidities (including mood disorders, anxiety disorders,disorders related with substance abuse, personality disorders and others) frequently associatedwith the development of eating disorders and response to treatment.Sociological studies on social values and eating disorders.Family studies on factors associated with the onset and maintenance of eating disorders and theimpact of these disorders on other family members.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS211

Annex 1. Levels of Evidence and Grades ofRecommendationSIGN Levels of Evidence and Grades of RecommendationLevels of Evidence1++ High quality meta-analysis, systematic reviews of clinical trials or high-quality clinicaltrials with low risk of bias.1+ Well conducted meta-analysis, systematic reviews of clinical trials, or well conductedclinical trials with low risk of bias.1- Meta-analysis, systematic reviews of clinical trials, or clinical trials with high risk of bias.2++ High quality systematic reviews of cohort or case-control studiesCohort or case-control studies with very low risk of bias and high probability ofestablishing a causal relationship.2+ Well conducted cohort or case-control studies with low risk of bias and moderateprobability of establishing a causal relationship.2- Cohort or case-control studies with high risk of bias and significant risk of non-causalrelationship.3 Non-analytic studies such as case reports, case series or descriptive studies.4 Expert opinion.Grades of RecommendationABAt least one meta-analysis, systematic review or clinical trial classified as 1++ anddirectly applicable to the guide’s target population, or a body of evidence composed ofstudies classified as 1+ with high consistency amongst them.Body of evidence composed of studies classified 2++, directly applicable to the guide’starget population and that have been shown to have high consistency amongst them, orevidence extrapolated from studies classified as 1++ or 1+.212CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

CBody of evidence composed of studies classified as 2+ directly applicable to theguide’s target population and that have shown to have high consistency amongstthem; or evidence extrapolated from studies classified as 2++.D Level 3 or 4 evidence or evidence extrapolated from studies classified as 2+.Good clinical practice *Recommended practice based on clinical experience and the consensus of thedrafting team.* Occasionally the working group becomes aware that there is an important practical aspect it wishes to emphasise and for which there probably is nosupporting evidence available. These cases are generally related with a certain aspect of the treatment that is considered good clinical practice andwhich would rarely be questioned. These aspects are considered good clinical practice points. These messages are not an alternative to evidence-basedrecommendations, and hence should be considered only when there is no other way to highlight the aspect in question. They are represented with the √symbol.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS213

Annex 2. Clinical chaptersAnnex 2.1. Spanish version of the SCOFF versionReproduced with the authors’ permission (J García-Campayo, 2004) 162Name: ______________________________________________________________________Sex: ________________________________________________________________________Age: ________________________________________________________________________1. Do you make yourself Sick because you feel uncomfortably full?YESNO2. Do you worry you have lost Control over how much you eat?YESNO3. Have you recently lost more than 6 kg in a 3 month period?YESNO4. Do you believe yourself to be Fat when others say you are too thin?YESNO5. Would you say that Food dominates your life?YESNO214CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Annex 2.2. Spanish version of the EAT-40Reproduced with the authors’ permission (J Castro, et al., 1991) 1741. I like to eat with other people.2. I prepare meals for others, but I don’t eat them.3. I get nervous when meal time approaches.4. I am very scared of weighing too much.5. I try not to eat even if I am hungry.6. I am very preoccupied with food.7. Sometimes I have engaged in bingeing, feeling I was unable to stop eating.8. I cut my food in small pieces.9. I take the calories of the food I eat into account.10. I especially avoid eating foods high in carbohydrates (for example, bread, rice, potatoes).11. I feel full after meals.12. I feel others would like me to eat more.13. I vomit after eating.14. I feel very guilty after eating.15. I am preoccupied with the desire to be thinner.16. I exercise a lot to burn calories.17. I weigh myself several times a day.18. I like wearing tight-fitting clothes.19. I like eating meat.20. I wake up early in the morning.21. I eat the same foods every day.22. I think about burning calories when I exercise.23. I have regular menstruation.24. Others think I am too thin.25. I am preoccupied with the idea of having body fat.26. I take longer to eat than other people.27. I like eating at restaurants.28. I take laxatives (purgatives).29. I try to eat only sugar-free food.215CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

30. I eat diet food.31. I feel food controls my life32. I exert self-control during meals.33. I notice others pressure me to eat.34. I spend too much time thinking and worrying about food.35. I have constipation.36. I feel uncomfortable after eating sweets.37. I commit to dieting.38. I like to feel an empty stomach.39. I enjoy trying new and tasty food.40. I feel like vomiting after meals.Answer categories:Never / Rarely / Sometimes / Often / Most of the time / Always.216CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Annex 2.3. Spanish version of the EAT-26Reproduced with the authors’ permission (A Gandarillas, et al., 2003) 170, 171 .1. I feel anxious about the idea of being too fat.2. I try not to eat when I am hungry.3. Food is a habitual preoccupation for me.4. I have experienced bingeing episodes in which I felt I could not stop eating.5. I cut my food in small pieces.6. I know the amount of calories contained in the foods I eat.7. I try not to eat foods that are high in carbohydrates (bread, rice, potatoes, etc.).8. I feel others would like to see me eat more.9. I vomit after eating.10. I feel very guilty after eating.11. I am obsessed with the desire to be thinner.12. When I play sports I think mainly about burning calories.13. Others think I am too thin.14. I am worried about having fat body areas and/or cellulite.15. I take longer than others to eat.16. I try to eat only sugar-free foods.17. I eat diet food.18. I feel my life revolves around food.19. I have good self-control over food.20. I feel others pressure me to eat more.21. I spend too much time thinking about food.22. I do not feel good after eating sweets.23. I am on a diet.24. I like to have an empty stomach.25. I like to try new food, tasty food that is high in calories.26. After meals I feel compelled to vomit.Answer categories:Always / Very often / Often / Sometimes / Rarely / Never.217CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Annex 2.4. Spanish version of the ChEATReproduced with the authors’ permission (M De Gracia, 2008) 173 .1. I am very scared of being overweight.2. I try not to eat even if I am hungry.3. I think about food constantly.4. I have sometimes engaged in bingeing, and felt I was unable to stop.5. I cut food in small pieces.6. I know how many calories are in the foods I eat.7. I avoid eating foods such as bread, potatoes or rice.8. I notice others would like me to eat more.9. I vomit after eating.10. I feel very guilty after eating.11. I am preoccupied with the desire to be thinner.12. I think about losing calories when I exercise.13. Others think I am too thin.14. I am worried about having body fat.15. I take longer than others to eat.16. I try to eat only sugar-free food.17. I notice others pressure me to eat.18. I spend too much time thinking and worrying about food.19. I feel uncomfortable after eating sweets.20. I commit to dieting.21. I like to feel an empty stomach.22. I enjoy trying new and tasty foods.23. I feel like vomiting after meals.24. I eat diet food.25. I feel food controls my life.26. I exert self-control during meals.Answer categories:Always / Most of the time / Often / Sometimes / Rarely / Never.218CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Annex 2.5. Spanish version of the BULITReproduced with the authors’ permission (AJ Vázquez, et al., 2007) 176 .Name:Date:Age: Current Weight: Height:Answer each of the following questions indicating the correct option with a cross. Please, respondtruthfully and remember that all information will be strictly confidential.1. Have you ever eaten uncontrollably to the point where you felt bloated?1. Once a month or less (or never)2. Two or three times a month3. Once or twice a week4. Three to six times a week5. Once a day or more2. I am satisfied with my eating behaviour1. Agree2. Neutral3. Slightly disagree4. Disagree5. Completely disagree3. Have you ever continued eating until you felt you were going to explode?1. Practically every time I eat2. Very frequently3. Often4. Sometimes5. Rarely or never4. Would you currently call yourself a big eater?1. Yes, completely2.Yes3. Yes, probably4. Yes, possible5. No, probably not5. I prefer eating1. At home alone2. At home with others3. At a public restaurant4. At friends’ houses5. It does not matter219CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

6. Do you feel you have control over the food you eat?1. Most of the time or all the time2. Often3. Occasionally4. Rarely5. Never7. I use suppositories or laxatives for weight management1. Once a day or more2. Three to six times a week3. Once or twice a week4. Two or three times a month5. Once a month or less8. I eat until I feel too tired to continue1. At least once a day2. Three to six times a week3. Once or twice a week4. Two or three times a month5. Once a month or less (or never)9. How frequently do you like to eat ice-cream, smoothies during a binging episode?1. Always2. Frequently3. Sometimes4. Rarely or never5. I do not overeat10. How concerned are you about bingeing?1. I do not binge2. I am not too concerned3. Moderate concern4. Intense concern5. It is probably the biggest concern of my life11. Most people I know would be surprised if they know how much food I eat every time I sitdown1. Absolutely2. Very probably3. Probably4. Possibly5. No12. Have you ever eaten until you felt sick?1. Very frequently2. Frequently3. Often4. Occasionally5. Rarely or never220CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

13. I am afraid of eating because I am afraid I will not be able to stop1. Always2. Most of the time3. Frequently4. Sometimes5. Rarely or never14. I do not feel good about myself after eating too much1. Always2. Frequently3. Sometimes4. Rarely or never5. I do not eat too much15. How frequently do you vomit intentionally after eating?1. Two or more times a week2. Once a week3. Two or three times a week4. Once a month5. Less than once a month (or never)16. How do you feel after bingeing?1. I do not binge2. I feel good3. I feel moderately disgusted with myself4. I feel pretty disgusted with myself5. I hate myself17. I eat a lot even when I am not hungry1. Very frequently2. Frequently3. Occasionally4. Sometimes5. Rarely or never18. My way of eating is different from the way of eating of most people1. Always2. Most of the time3. Frequently4. Sometimes5. Rarely or never19. I have tried to lose weight by fasting or intense dieting1. Not in the past year2. Once in the past year3. Two or three times in the past year4. Four or five times in the past year5. More than five times in the past year221CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

20. I feel sad after eating more than I intended to eat1. Always2. Most of the time3. Frequently4. Sometimes5. Rarely, never or it is not the case21. When I binge I tend to eat foods high in carbohydrates(sugars, starch)1. Always2. Most of the time3. Frequently4. Sometimes5. Rarely, or I do not overeat22. Compared to most people, my ability to control my eating behaviour seems to be:1. Greater than others’2. More or less the same3. Lesser4. Much lesser5. I have no control whatsoever23. One of your best friends suddenly suggests that you both have dinner at a new restaurant thatevening. Although you had planned to eat lightly at home, you go out for dinner, eat quite alot and feel uncomfortably full.How would you feel about yourself on the way home?1. Good, happy about trying a new restaurant2. Slightly bad about eating so much3. Somewhat frustrated with yourself4. Disgusted with yourself5. Totally disgusted with yourself24. At present I could consider myself a “compulsive eater” (who has episodes of uncontrolledeating)1. Absolutely2. Yes3. Yes, probably4. Yes, possible5. No, probably not25. What is the most weight you have lost in a month?1. More than 20 kg2. 12-20 kg3. 8-11 kg4. 4-7 kg5. Less than 4 kgCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS222

26. If I eat too much at night, I feel depressed the following morning1. Always2. Frequently3. Sometimes4. Rarely or never5. I do not eat too much at night.27. Do you think it is easier for you to vomit than for most people?1. Yes, I do it effortlessly2. Yes, it is easy for me3. Yes, it is a bit easier for me4. More or less the same5. No, it is less easy for me28. I feel food controls my life1. Always2. Most of the time3. Frequently4. Sometimes5. Rarely or never29. I feel depressed right after eating too much1. Always2. Frequently3. Sometimes4. Rarely or never5. I do not eat too much30. How frequently do you vomit after eating trying to lose weight?1. Less than once a month (or never)2. Once a month3. Two-three times a month4. Once a week5. Twice or more times a week31. When you eat a large amount of food, how fast do you usually it eat?1. Faster than anyone ever has2. Much faster than most people3. A bit faster than most people4. Like most people5. Slower than most people (or not applicable)32. What is the most weight you have gained in a month?1. More than 20 kg2. Between 12-20 kg3. Between 8-11 kg4. Between 4-7 kg5. Less than 4 kg223CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

33. APPLICABLE ONLY TO WOMEN. My last period was1. One month ago2. Two months ago3. Four months ago4. Six months ago5. Over six months ago34. I use diuretics to help manage my weight1. Once a day or more2. Three to six times a week3. Once or twice a week4. Two or three times a month5. Once a month or less (or never)35. What do you think of your appetite compared to that of most people you know?1. Often bigger than most2. Much bigger3. A bit bigger4. More or less the same5. Smaller than most36. APPLICABLE ONLY TO WOMEN. I have my period once a month1. Always2. Generally3. Sometimes4. Rarely5. NeverPC 1 10 20 30 40 50 60 70 80 90 99TOTALExc_____________________Sen ____________________Vom____________________Foo ____________________Wei ____________________224CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Annex 2.6. Spanish version of the BITEReproduced with the authors’ permission (T Rivas, et al., 2004) 181 .1. Do you have a regular daily eating pattern? YES NO2. Are you a strict dieter? YES NO3. Do you experience feelings of failure when you break a diet,even if you only do so once? YES NO4. Do you count the calories in everything you eat, even if you arenot on a diet?YES NO5. Have you ever fasted for one whole day? YES NO6. ... if you have responded «YES» to question 5, how frequently doyou do so? Alternate days 2-3 times a week Once a week OccasionallyJust once543217. Do you use any of the following methods to lose weight? (Draw a circle around each answerbased on the frequency, in accordance with the table below).WEIGHT-LOSS PILLS 0 2 3 4 5 6 7USE OF DIURETICS 0 2 3 4 5 6 7USE OF LAXATIVES 0 2 3 4 5 6 7SELF-INDUCED VOMITING 0 2 3 4 5 6 7-Never-Occasionally-Once a week-2 or 3 times a week- Daily- 2 or 3 times per day- 5 or more times a day 78. Do your eating habits severely disrupt your life?0234567YES9. Do you feel that food controls your life? YES NO10. Do you ever eat and eat until you are stopped byphysical discomfort? YES NO11. Are there times when all you can do is think aboutfood? YES NONOCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS225

12. Do you eat reasonable amounts of food in front ofothers and then binge in secret? YES NO13. Are you able to stop eating when you wish?14. Do you ever experience an OVERWHELMING desireto eat and eat?15. Do you tend to eat a lot when you feel anxious?16. Are you TERRIFIED of the idea of becoming obese?17. Do you ever eat large amounts of food (not only duringmeals)?18. Do you feel ashamed of your eating habits?19. Do you worry that you have lost control over howmuch you eat?20. Do you turn to food for comfort?21. Are you able to leave food on your plate at the end of ameal?22. Do you deceive other people about how much you eat?23. Do the amounts you eat directly depend on the hungeryou are experiencing?24. Do you always binge?25. ... if you have answered «YES», do you despise yourselfwhen you binge?26. If you do binge, do you only do it when you are alone?27. If you do binge, how often do you do so?2-3 times a day 6Daily 52-3 times a week 4Once a week 3Once a month 2Rarely 1YESYESYESYESYESYESYESYESYESYESYESYESYESYESYESNONONONONONONONONONONONONONONO28. Would you do anything to satisfy the overwhelmingdesire to binge?YESNO226CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

29. If you binge eat, do feel very guilty?30. Do you ever eat in secret?31. Do you think your eating habits are normal?32. Do you consider yourself a compulsive glutton?33. Does your weight change more than 2.5 kg per week?YESYESYESYESYESNONONONONO227CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Annex 2.7. Diagnostic Criteria for Eating DisordersICD-10 Diagnostic Criteria for Eating DisordersIn 1992 the WHO published the ICD (International Statistical Classification of Diseases andRelated Health Problems). The ICD is used worldwide for statistics on morbidity and mortality,reimbursement systems and automatic decision support in medicine. This system is designed topromote international comparison of the recollection, processing, classification and presentationof these statistics.At this moment, the classification currently in vigour is the tenth edition (ICD-10) and theWHO continues to work on it, publishing minor annual updates and bigger updates every threeyears.Anorexia nervosa (F50.0)Disorder characterised by the presence of deliberate weight loss, induced or sustained by thepatient. The disorder occurs most frequently in adolescent girls and young women, although onrare occasions it may affect adolescent boys and young men, as well as prepubertal children orolder women up to the menopause. AN constitutes an independent syndrome, in the followingsense:a) The syndrome’s clinical features are easily recognized, resulting in a reliable diagnosis witha high degree of agreement between clinicians.b) Follow-up studies have demonstrated that, amongst patients who do not recover, aconsiderable number continue to show the main characteristics of AN in a chronic form.Despite the fact that the main causes of AN remain elusive, there is growing evidence suggestingthat there are a series of sociocultural and biological factors that interact and contribute to theonset of AN, in which less specific psychological mechanisms and personality vulnerability alsotake part. The disorder is accompanied by malnutrition of varying severity, leading to endocrineand metabolic disturbances and other functional disorders. It remains uncertain whether thecharacteristic endocrine disorder is entirely due to malnutrition and the direct effect of thebehaviours that have caused it (for example, restricted dietary choice, excessive physicalexercise with metabolic balance disturbances, self-induced vomiting and laxative abuse, with theresulting electrolyte imbalances) or if other yet unknown factors are involved.Diagnostic Guidelines:All the following disturbances must be present:a) Significant weight loss (BMI

c) Body image distortion that consists of a specific psychopathology characterised by a dreadof fatness and flaccidity of body areas that persists as an intrusive, overvalued idea, leadingthe patient to impose a low weight threshold on himself or herself.d) A widespread endocrine disorder that affects the hypothalamic-pituitary-gonadal axismanifesting in women as amenorrhoea and in men as loss of sexual drive and potency (Anapparent exception is the persistence of vaginal bleeds in anorexic women who arereceiving replacement hormonal therapy, most commonly taken as a birth control pill).There may also be elevated levels of growth hormone and cortisol, changes in theperipheral metabolism of the thyroid hormone, and insulin secretion abnormalities.e) If onset occurs before puberty, the sequence of pubertal events is delayed or even stunted(growth ceases; in girls the breasts do not develop and there is a primary amenorrhoea; inboys the genitals remain juvenile). If recovery takes place, puberty is often completednormally, but the menarche is late.Excludes:Anorexia, loss of appetite (R63.0).Psychogenic anorexia (F50.8).Atypical Anorexia Nervosa (F50.1)This term must be used in cases where one or more key features of AN (F50.0), such asamenorrhoea or significant weight loss, are missing, but that otherwise present a rathercharacteristic clinical picture. These types of patients are more frequent in consultative andliaison psychiatry and in primary care. Patients who present all key symptoms of AN in a milddegree an also be included in this group. This term must not be used for eating disorders thatresemble AN but that are actually a result of a known physical ethiology.Diagnostic Criteria for Bulimia Nervosa (F50.2)Syndrome characterised by repeated episodes of binge-eating and excessive preoccupation withthe control of body weight, leading the patient to use extreme measures to mitigate the weightgain caused by ingested food. This term should be limited to the forms of the disorder that arerelated to AN by virtue of sharing the same psychopathology.The age and sex distribution is similar to that of AN, but the age of presentation tends to beslightly later. The disorder may be considered a sequel to persistent AN (although the reversesequence may also occur). At first glance, a previously anorexic patient may appear to improveas a result of weight gain and menstruation may even return in the case of a female, but aharmful pattern of behaviour characterised by overeating and self-induced vomiting thenbecomes established. Repeated self-induced vomiting is likely to give rise to disturbances ofelectrolyte balance, physical complications (litany, epileptic seizures, cardiac arrhythmias,muscular weakness), and greater loss of weight.Diagnostic Guidelines:All the disturbances listed below must be present, thus constituting strict diagnostic guidelines.229CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Within each guideline some variations can be accepted, as is indicated:a) There is a persistent preoccupation with eating, and an irresistible craving for food; thepatient succumbs to episodes of overeating in which large amounts of food are consumed inshort periods of time.b) The patient attempts to counteract the weight gain caused by ingested food by one or moreof the following methods: self-induced vomiting; laxative abuse, alternating periods offasting; use of drugs such as appetite suppressants, thyroid preparations or diuretics. Whenbulimia occurs in diabetic patients they may choose to neglect their insulin treatment.c) The psychopathology consists of a morbid dread of fatness and the patient sets herself orhimself a sharply defined weight threshold, well below the premorbid weight thatconstitutes the optimum or healthy weight. There is often, but not always, a history of anearlier episode of AN, the interval between the two disorders ranging from a few months toseveral years. This earlier episode may have been fully expressed, or may have assumed aminor cryptic form with a moderate loss of weight and/or a transient phase of amenorrhoea.Include:Bulimia NOS (not otherwise specified).Hyperorexia nervosa.Diagnostic criteria for atypical bulimia nervosa (F50.3)This term must be used in cases where one or more key features of BN (F50.2) are missing butthat otherwise present a rather typical clinical picture. Patients frequently have normal weight orare even slightly overweight, but they present repeated bouts of overeating followed by selfinducedvomiting or purging. Partial syndromes accompanied by depressive symptoms are notuncommon (if these symptoms fulfil the guidelines of a depressive disorder a double diagnosismust be made).Includes:Bulimia with normalweight.Diagnostic Criteria for Other Eating Disorders (F50.8) and UnspecifiedEating Disorders (F50.9)Other eating disorders must be coded using the ICD-10 F50.8 code (other eating disorders).Unspecified eating disorders must be coded using the F50.9 code (Unspecified eatingdisorders).DSM-IV-TR Diagnostic Criteria for Eating DisordersThe DSM-IV (Diagnostic and Statistical Manual of Mental Disorders IV) of the APA(American Psychiatric Association) is a classification of mental disorders that was elaboratedwith the objective of providing clear descriptions of diagnostic categories, to enable cliniciansand researchers to diagnose, study and Exchange information and address different mental230CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

disorders. In 1994, the fourth version, the DSM-IV, was published. The latest version, theDSM-IV-TR, which is currently in use, was published in 2000 and includes some revisions. Atpresent the APA is developing the upcoming DSM-V, the publication of which is expected to bein 2011.The DSM is an instrument based on empirical data and presenting in the form ofdescriptive methodology with the aim of improving communication between clinicianspertaining to different orientations and between clinicians in general with different researchers.Thus, it does not try to explain different pathologies, or to propose pharmacological orpsychotherapeutic treatment guidelines or specific branches within psychology or psychiatry. Itis important to clarify that professionals with clinical experience must always use it given that itis used as a guide that must be accompanied with the necessary clinical judgement, professionalknowledge and ethical criteria.The DSM-IV is a diagnostic tool that presents a description of the current functioning ofthe patient by means of five “axes”, with the aim of providing a general view of differentfunctional areas.Anorexia nervosa (307.1)Diagnostic Criteria:a) Refusal to maintain body weight at or above a minimally normal weight for age and height:(for example, weight loss leading to maintenance of body weight

Bulimia nervosa (307.51)Diagnostic Criteria:a) Recurrent episodes of binge eating. An episode of binge eating is characterized by:1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of foodthat is definitely larger than most people would eat during a similar period of time andunder similar circumstances.2. A sense of lack of control over eating during the episode (e.g., a feeling that one cannotstop eating or control what or how much one is eating).b) Recurrent inappropriate compensatory behaviour in order to prevent weight gain, such asself-induced vomiting; misuse of laxatives, diuretics, enemas, or other medications; fasting;or excessive exercise.c) The binge eating and inappropriate compensatory behaviours both occur, on average, atleast twice a week for 3 months.d) Self-evaluation is unduly influenced by body shape and weight.e) The disturbance does not occur exclusively during episodes of AN.Specify type:– Purging Type: during the current episode of BN, the person has regularly engaged in selfinducedvomiting or the misuse of laxatives, diuretics, or enemas.– Non-purging Type: during the current episode of BN, the person has used otherinappropriate compensatory behaviours, such as fasting or excessive exercise, but has notregularly engaged in self-induced vomiting or the misuse of laxatives, diuretics, orenemasEDNOS (307.50)The EDNOS category refers to eating disorders that do not satisfy criteria for any specific eatingdisorders. For example:• In women, all diagnostic criteria for AN are met, but menstruation is regular (EDNOS 1).• All diagnostic criteria for AN are met but despite substantial weight loss, the patient’sweight is in the normal range (EDNOS 2).• All diagnostic criteria for BN are met except binges and inappropriate compensatorybehaviours occur at a frequency of less than twice a week or for a duration of less than 3months. (EDNOS 3).• All diagnostic criteria for BN are met, except an individual of normal body weight engagesin the regular use of inappropriate compensatory behaviours after eating small amounts of232CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

food (for example, self-induced vomiting after eating two cookies) (EDNOS 4).• Chew and spit out, but not swallow, large amounts of food.• Compulsive disorder: characterised by repeated episodes of binge eating in the absence ofinappropriate compensatory behaviours typical of BN.Though the DSM-IV includes research criteria for later studies, BED remains classified in eatingdisorders not otherwise specified.Table 1. Comparison of diagnostic criteria: DSM-IV, ICD-9, ICD-10DiagnosisDiagnostic ClassificationsDSM-IV-TR ICD-9 ICD-10Anorexia nervosa 307.1 307.1 F50.0Bulimia nervosa 307.51 307.51 F50.2Unspecified eating disorders 307.50 307.50 F50.9233CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Annex 2.8. Spanish version of the EDE-12 semistructuredinterview (R M Raich) 191The twelfth edition of Fairburn and Cooper’s, 1993 190 semistructured interview (EDE-12) is theresult of the gradual improvement of the interview originally designed by Cooper and Fairburnin 1987. The current version can now be used for the diagnosis of eating disorders based onDSM-IV criteria, to assess the frequency of serious behaviours present in eating disorders andthe severity of other important aspects of the psychopathological characteristics of eatingdisorders. The EDE-12 consists of 62 items that assess 4 subscales: restraint, preoccupation withfood and preoccupation with shape. Each of the patient’s answers is evaluated by theinterviewer on a scale of 0 to 6 points that determine intensity or frequency. Scores can beobtained for items, subscales and also an overall severity score. Although it was designed toassess the symptoms of eating pathology in the last four weeks and focuses on them, it was latermodified so it could be used to assess the presence of these symptoms in the last three months 192,193.Annex 2.9. Incorrect ideas about weight and health 10– Any kind of fat in food is bad.– It is healthy to be thin.– Fat can be lost quickly and without posing a risk to health.– In women there is a special kind of fat called cellulite.– Cellulite is caused by toxins.– The fat in a certain body area can be reduced (hips and thighs).– Certain foods, or combination of foods, can activate metabolism and accelerateweight loss.– Obese women under the age of 50 are at risk for heart disease.– Dieting is a healthy activity.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS234

Annex 2.10. Description of proposed indicatorsProportion of patients with eating disorders who have beenadequately referred to a specialised level of careCriteria for referralfrom PC to mentalhealth services (MHCFAand MHSFCA)– When there is an established diagnosis of eating disorder.– Weight loss equal to or higher than 10%-25% of weight,without a justifiable cause.– Presence of regular bulimic episodes, meaning binge-eatingbehaviour and/or persistent purging practices (self-inducedvomiting, laxative abuse and use of diuretics).– Presence of associated psychopathological disturbances.– Lack of disease awareness.– If neither weight nor bulimic behaviour improve afterfollowing PC guidelines.Preferential cases (1-3 days) and other cases (max. 1 month).Formula:Patients with eating disorders who have been adequatelyreferred to a specialised level of care / patients with eatingdisorders x 100.Standard:To be determined.Proportion of patients with eating disorders adequately referred withemergency criteriaCriteria for referral fromPC to emergencyhospitalisation:– Weight loss >50% in the last 6 months (30% in the last 3months).– Consciousness disturbances.– Convulsions.– Dehydration.– Severe liver or kidney disturbances.– Pancreatitis.– Decreased potassium

Formula:Patients with eating disorders adequately referred withemergency diagnosis / patients with eating disorders referredwith emergency diagnosis x 100.Standard:To be determined.Proportion of patients who receive diagnostic confirmation within two months ofthe first consultationAppropriate timeinterval:Except in high risk situations, all patients with eatingdisorder shall have the diagnosis and individual therapeuticplan established within two months of the first consultation.Formula:Patients who have been diagnosed in the appropriate timeframe /patients diagnosed with an eating disorder x 100.Standard:To be determined.Percentage of general hospital readmissions at 3, 6, 9 and 12 monthsFormula:Number of patients who are discharged from a generalhospital due to eating disorders, at 3 months-total number ofdischarges in that time frame / total number of discharges toa general hospital in that same time frame due to mentaldisorder x 100.Definitions:Levels of disaggregation:Sources of information:Periodicity:Clarifications:All discharges classified in the ICD-10 will be included(codes F50.0, F50.1, F50.2, F50.3; F50.8 and F50.9 of the10th version).Per autonomous community.Registry of hospital discharges (MBDS)-MSC (Ministry ofHealth and Consumer Affairs).3, 6, 9, 12 months (to be determined).Discharges from general hospitals will be counted. Thenumerator is currently biased by not being able to identifypatients who have been discharged from different hospitalsuntil all databases of the individual health care card ofautonomous communities of the NHS are integrated.236CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Proportion of patients seen with the diagnosis of eating disorder in PC, adultand children’s MHC (MHCFA –MHCFCA), day hospital and general hospitalFormula:Definitions:Levels of disaggregation:Sources of information:Number of patients diagnosed with an eating disorder/totalpopulation x 100.Prior agreement of the autonomous communities on registerand coding criteria of cases managed on an outpatient levelby mental health specialised services is required. Alladmissions classified in the ICD-10 will be included (codesF50.0, F50.1, F50.2, F50.3; F50.8 and F50.9 of the 10 thversion).According to type of eating disorder, level of care (PC,MHC, day hospital and general hospital), autonomouscommunity, age and sex.Death statistics and population projections. NSI.Periodicity:Observations:Annual.At present there are no data for the entire NHS. It requiresthe previous agreement of normalised registry criteria andsubsequent sharing of information by the MSC.Satisfaction index of patients and family members by the end of treatmentFormula:Definition:Levels of disaggregation:Periodicity:Clarifications:Number of surveyed individuals who deemed all aspectsto be adequate / total number of surveyed individuals x100.All patients treated in primary and specialised care foreating disorders will be included at the end of treatment.According to type of eating disorder, autonomous communityand age and sex groups.Annual.Only those individuals who refuse to complete thequestionnaire will be excluded. Returned questionnaires andthe characteristics of those who answered and those who didnot will have to be reported. Expected response rate is 50%.237CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Annex 3. Information for patients with eating disordersand their familiesAnnex 3.1. Patient InformationEating Disorders. What should you know?This information will help you gain deeper knowledge on eating disorders and understand theimportance of becoming involved in treatment and in the recovery process. The aspectsaddressed are the definition of these disorders, their symptoms and course and recommendedtreatments based on available research results.Eating DisordersWhat are eating disorders?People with eating disorders are characterised by adopting maladaptive eating behaviours as aresponse to personal body image dissatisfaction. They frequently present distorted thoughts onweight (they feel inferior to others, and believe they are negatively judged due to their physicalappearance) and health (fat in food is harmful, it is healthy to be thin, weight can be lost quicklywithout posing any risks to health, dieting is a healthy activity, etc). People with these disorderssuffer nutritional, physical, psychological and social consequences. If left untreated, thesedisorders can be life-threatening.These eating problems can affect all people, regardless of their socio-economic or culturalsituation. Eating disorders are more common in females (90-95%), but lately there has been agrowing incidence in men. These disorders can occur at any age, but most commonly develop inadolescence due to the vital changes that take place during this time and the search for selfidentityit entails. In the past few years earlier and earlier ages of onset of eating disorders havebeen observed. It is a process that can initiate very subtly and remain initially undetected.In general, people with anorexia nervosa (AN) and bulimia nervosa (BN) share anexcessive preoccupation with losing weight, even if they have normal weight or even if theirweight is well below the healthy standard. Food becomes the main focus of their concern andother aspects of life are gradually neglected.AN and BN differ in the way people react to food and the different physical consequencesthat result. If adequate treatment is not followed, one disorder may lead to another.What is anorexia nervosa?AN is characterised by excessive dread of becoming fat and by a distortion of body imagethat leads patients to feel and view themselves as fat when in fact they are not. They refuse tomaintain their weight within a normal range and to this end they impose dietary restrictions onthemselves to lose weight. Their self-evaluation is determined by how they see their body andCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS238

shape. Perfectionism and low self-esteem are common. Often depression and obsessivethoughts are also part of the disorder. Individuals with AN rarely seek help and hide theirsymptoms for as long as they can.What is bulimia nervosa?In the case of BN, individuals engage in bouts of eating large amounts of food (bingeing)and subsequently carry out activities to maintain their weight. This behaviour can take over theirdaily life and hamper social relations and interactions. Individuals with BN usually hide theirbehaviour and rarely seek help. They may have a normal weight, or, paradoxically, becomeoverweight as a result of their inadequate eating behaviours. The fear of gaining weight andsense of lack of control over eating determine their mood and mental state, which can result indepressive processes.What are atypical eating disorders?These eating disorders are called atypical because they do not entirely fit into the clinicaldefinition of AN or BN due to the absence of one of the key symptoms of these disorders.Individuals with these disorders may present a combination of AN and BN symptoms that mayvary over time. Many people with atypical eating disorders have suffered AN or BN in the pastor will develop in the future.The most well known atypical eating disorder is binge-eating disorder. In this disorder,patients engage in bingeing episodes, but do not try to control their weight by means of purgingpractices. They may feel anxious, tense and depressed, with the resulting impairment of theirsocial life and relationships.Atypical disorders, included binge-eating disorder, account for more than half the cases ofeating disorders.What is the origin of eating disorders?There are many predisposing factors in the development of eating disorders: biologicalpredisposition which includes genes, society (pressure to be thin as a symbol of beauty andsuccess), family environment (tense, distant, cold, overprotective, uncommunicative climate,high family expectations, parents’ excessive preoccupation with weight and diet,, obesity in thefamily) and personal character (maturity fears, perfectionism and self-control or low self-esteemand personal dissatisfaction).Experiencing certain situations can trigger the disorder. For example, puberty, stressfulsituations (physical or psychological abuse, loss of a family member, separation or divorce,relocation, adaptation difficulties, exams, etc.), comments and pressure to lose weight, lowcaloriediets, succumbing to the cultural stereotype and adherence to mass media messages,including Internet, which promote an abnormal image of thinness, excessive exercise, etc.Once the disorder has been triggered, some of its consequences serve its maintenance andlead to further deterioration (for example, the biological consequences of malnutrition, socialalienation and mood problems).239CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Alert SignsWhat signs can alert us to a possible eating disorder?There are several changes that help detect the presence of the disorder, of which the followingshould be highlighted:In relation to eatingFeeling of guilt for eating or not eating; preferring to eat alone, eating reduced amounts of food,presence of bingeing in the last few weeks, the feeling of not being able to stop eating,continuous avoidance of certain foods (for example, sweets), consumption of low-calorie andhigh-fibre foods, use of diuretics and laxative abuse, self-induced vomiting and dietary restraintor fasting.In relation to body imageExcessive preoccupation with body or shape, the belief that physical appearance is very valuableas a conduit to gain success in any aspect of life, excessive adherence to cultural stereotypes anddepending on certain magazines for their advice on dieting, weight or figure.In relation with physical exerciseExcessive physical exercise and restlessness if it is not performed, use of exercise to lose weight.In relation with behaviourConstant personal dissatisfaction, depressive and irritable state, frequent mood changes;decreased social relations with increasing alienation, apparent increase of study hours, difficultyconcentrating and regular visits to websites, blogs or chats that preach thinness and give outadvice on losing weight or purging.What are the consequences of inadequate eating behaviour?The adoption of inadequate eating behaviours lead to physical disturbances in the patient, whichare different in the case of AN versus BN:In anorexia nervosaUnexplainable weight loss or stunted weight (in children), delayed menarche or loss ofmenstruation, paleness, hair loss, feeling cold, blue fingers, appearance of lanugo, low bloodpressure, arrhythmia, weakness and dizziness.In bulimia nervosaIrregular periods, muscle pain and fatigue, chronic throat irritation or loss of teeth due torepeated self-induced vomiting and inflammation of salivary glands.Where can we seek professional help?If you think you may be suffering from an eating disorder, it is very important that you seekhelp. Management of this type of disease begins in your primary care centre, where the generalpractitioner or paediatrician will advise you and assess your case. In certain circumstances, theCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS240

team of psychiatrists, psychologists, etc. of the mental health centre/unit in your area will undertakeyour management to resolve the problem. There are also hospitalisation units (reference) tomanage those patients who, due to the severity of their situation, require day care or inpatient care.Do not worry about confidentiality. All specific details that you share with health careprofessionals are personal and private information and will not be disclosed.TreatmentThe family’s collaboration is essential in the treatment of these diseases. Treatment mustbe carried out by multidisciplinary teams of specialised professionals who can manage themedical, psychological, social and family complications that may arise. Medical care is aimed ateliminating physical complications, restoring normal weight and learning about following ahealthy diet.Once the necessary physical balance has been achieved, psychic problems linked to thedisease are addressed. Psychologists or psychiatrists will be in charge of these therapies. Thus,proper treatment of these disorders should take the following aspects into consideration:Psychological treatment: aimed at modifying distorted thoughts and negative feelings regardingweight, shape and body size in the patient’s systems of values to help construct or recover anidentity that aids the person in coping with life’s challenges and difficulties.This treatment can be delivered individually or in group sessions with other patients whoare experiencing the same problems and, in some cases, with family members (parents, siblings,spouse, etc.).Nutritional treatment: its main objective is to provide counselling on healthy eating habits andto provide information on the dangers of following unnecessary diets that, although justifiable,are not prescribed or managed by a competent health care professionals.The social dimension of food, understood in terms of how eating provides a pleasantopportunity for family interaction, is emphasised more than food’s nutritional value. It isimportant to receive nutritional counselling from the beginning of treatment to prevent relapses.Pharmacological treatment: aimed at patients who require drugs in combination withpsychological treatment, especially in cases of BN and BED, or to resolve associatedsymptomatology such as depression, anxiety or impulsiveness.Not all patients are the same or require the same treatments. That is why it is important foryou to follow your health practitioner’s advice and to get involved in your own treatment.Eating disorders have varying degrees of severity. Treatment can be performed on anoutpatient basis, although in very severe cases temporary hospitalisation (inpatient or day care)may be necessary.National associations of individuals with eating disordersAside from the resources available in the NHS to address these diseases, patients and family241CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

members can seek support and guidance in associations (share experiences, listen to othertestimonials, obtain support and professional counselling thanks to experts who collaborate withthese associations, etc). Some of these associations are:• Association in Defence of Anorexia Nervosa and Bulimia Management [Asociación enDefensa de la Atención de la Anorexia Nerviosa y Bulimia (ADANER)]http://www.adaner.org• Spanish Federation of Support Associations for Anorexia and Bulimiahttp://www.feacab.org(FEACAB)Annex 3.2. Support associations for patients with eating disordersand their family membersAssociation in Defence of Anorexia Nervosa and BulimiaManagement (ADANER)]ADANER is an association of patients with eating disorders and their families. Its activity iscarried out all over the country by its delegations and support groups. Its objectives are based onimproving the care and quality of life of patients and their family members, disseminatinginformation and making society aware of all aspects related to these diseases, and preventing andsupporting research in this field.e-mail: info@adaner.org web: http://www.adaner.orgTelephone Number: 915 77 02 61Spanish Federation of Support Associations for Anorexia andBulimia(FEACAB)FEACAB is composed of associations from different Spanish provinces or autonomouscommunities and more than 20,000 people with AN and BN and their families. Its objectives arebased on promoting the existence of sociosanitary and educational solutions that are adequateand sufficient for the prevention and treatment of these diseases, promoting good practicestandards, for both associations and other groups –mass media, commerce, etc.- and addingprevention efforts that are already being carried out by each association.e-mail: arbada@arbada.org web: http://www.feacab.orgTelephone number: 976 38 95 75CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS242

Annex 4. GlossaryCounsellingPerformance of several personal interviews with patients and family members which serve toinform and educate on the disease and its main sanitary, family and social consequences, and toprovide insight on the current situation of health care, legal, economic and social resources withthe aim of reassuring and assisting the patient and/or family.AlprazolamBenzodiazepine that produces its effect by binding stereospecific receptors located in the NCS.The following therapeutic indications have been approved in Spain: generalised anxiety anddepression-related anxiety, and anxiety disorders with or without agoraphobia.Benzodiazepines are only indicated in the treatment of an intense disorder that limits the patient’sactivity or subjects him/her to significant stress.AmitriptylineTricyclic antidepressant. The following therapeutic indications have been approved in Spain:treatment of depression and chronic neuropathic pain.AtomoxetinePsychostimulant drug. The following therapeutic indications have been approved in Spain:treatment of attention deficit disorder with hyperactivity (ADDH) in children >6 years andadolescents as part of a complete treatment programme.“Pure” Self-Help (SH)Intervention that employs a clear model and treatment structure and includes all necessaryinstructions on how the user can improve his/her skills to assess and manage difficulties. Materialcan be found in any format, including books, CD-ROM, Internet packages, etc.; it can beindividual or group-based; psychoeducational material can be included depending on itsobjectives, that is, to alleviate symptoms vs. improving knowledge.Guided Self-Help (GSH)It is the previously defined self-help (SH) and contact with a “therapist” who may be a mentalhealth professional or a non-specialised individual. This intervention does not include:exclusively educational prevention material; pure support groups (since it does not considerimproved clinical outcome a direct objective); groups that do not focus their sessions on onerecognisable tool, for example: book, CD-ROM, video; sessions where the emphasis lies on theCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS243

therapist who guides the sessions and is present in most of the “action”. The number of hours ofguidance can vary.BrofamineAntidepressant belonging to the group of monoaminooxidase inhibitors (MAOI). It does notappear in the Vademecum or in the AGEMED (Spanish Drug Agency). It has been used in thecontrol group of several RCTsCyproheptadineIt belongs to the group of antihistamines (which block histamine H1 receptors). Aside fromblocking the action of histamine H1 receptors in the brain, alleviating allergic reaction symptoms,cyproheptadine can also block serotonin receptors in the brain, thus stimulating appetite. Thefollowing therapeutic indications have been approved in Spain: anorexia, prevention andsymptomatic treatment of nutrient-deficient states in convalescent periods or inadequate dietaryintake. Appetite and development stimulant.CitalopramAntidepressant belonging to the group of SSRIs. The following therapeutic indications have beenapproved in Spain: major depressive episodes, prevention of depression relapse/recurrence, anxietydisorder with or without agoraphobia and OCD.ClomipramineTricyclic antidepressant. The following therapeutic indications have been approved in Spain: anykind of depression, symptomatology and severity, obsessive syndromes, phobias, panic attacks,narcoleptic syndromes with cataplexy crises, nocturnal enuresis (only after 5 years of age and afterruling out organic causes).Nutritional CounsellingDietary or nutritional counselling or nutritional therapyType of treatment in which the main objective is to modify what the patient eats, and his/herhabits and attitudes towards food. It is not a clearly defined intervention and it is applied inseveral modalities. It consists of providing a model which involves following a series ofindications such as eating a healthy diet, maintaining fixed eating schedules, eating 3 meals a day,eating normal rations depending on age, eating while sitting down with the family, in a relaxedenvironment without distractions, without preparing the meal and resting after eating. Weightrestoration requires a normocaloric, healthy diet, except in cases in which it is contraindicated dueto the patient’s condition.Media literacyPrimary prevention interventions based on cognitive behaviour and inoculation theories that aimto reduce risk factors of eating disorders by means of learning activities that enable the acquisition244CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

of skills to fend off social persuasion. The approach aims to prepare participants to adopt acritical assessment of media content so they can identify, analyse, challenge and proposealternatives to cultural ideals presented in the mass media. Videos are played and then discussedto broaden knowledge and stimulate critical analysis of the group participants.DesipramineTricyclic antidepressant. It is not included in the Vademecum or in the AGEMED (Spanish DrugAgency). It has been identified as treatment in the control group of some RCTsPhenelzineAntidepressant belonging to the MAOI group, which has been withdrawn from the Spanishmarket.FluoxetineAntidepressant belonging to the group of SSRIs. The following therapeutic indications havebeen approved in Spain: major depression, OCD and BN.FluvoxamineAntidepressant belonging to the group of SSRIs. The following therapeutic indications have beenapproved in Spain: depression and OCD.Mutual help groups (MHGs)Groups of people who meet voluntarily with the aim of helping each other. They are generallycomprised of individuals who share the same problem or who find themselves in a similardifficult situation. The MHG emphasises personal interaction and each member’s capacity toassume responsibilities. It tends to provide emotional help and promote values that help membersstrengthen their own sense of self. These groups provide assistance and emotional support tofamilies and patients, facilitating the success of the corresponding therapy. Groups are guided byfacilitators (people who have experienced the same problem or situation as the participants) andare periodically aided by a professional who supervises the intervention and provides instrumentsto improve group dynamics.ImipramineTricyclic antidepressant. The following therapeutic indications have been approved in Spain:depression and nocturnal enuresis in children.Interventions aimed at eliminating risk factors of the disorder (in this case, eating disorders)Primary prevention interventions that can be specific or non-specific depending on theissue/aspect that is being addressed, providing participants with certain skills to cope withproblems (management skills). Specific interventions are focused on: age of onset, child obesity,CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS245

negative attitudes towards weight and shape, irrational beliefs on the benefits of being on a diet,social pressure to manage weight, dieting, amongst others. Non-specific interventions address:risk exposure, psychopathology of parents, lack of parental bond, physical and/or psychologicalabuse by family members, amongst others. Discussions/debates are carried out in classrooms,programmed sessions, etc.Interventions aimed at making the patient stronger to tackle the disease (in this case, eating disorders)Primary prevention interventions. Protection is achieved by providing the patient (host) withdifferent skills (life skills, skills to deal with social pressure, to solve problems, etc.) andperforming activities to develop coping skills. Discussions/debates are carried out in classrooms,programmed sessions, etc.Psychoeducational interventionsPrimary prevention interventions that consist of communicating information on a certain matter(in this case, on eating disorders), which will later be the central topic of debate/discussionbetween group participants.LithiumMood stabilising psychoactive drug. The following therapeutic indications have been approved inSpain: prophylaxis and treatment of manic-depressive psychosis, recurrent unipolar depression,endogenous depression resistant to standard treatment, neutropenia following treatment withcytostatics, medullary aplasia and Felty’s syndrome.LorazepamBenzodiazepine that binds with specific receptors in several locations of the NCS, boosting theeffects of synaptic or presynaptic inhibition mediated by GABA or directly affecting the potentialaction of generation mechanisms. The following therapeutic indications have been approved inSpain: short-term treatment of all states of anxiety or tension, associated or not to functional ororganic disorders, psychic disturbances, psychosomatic diseases, organic diseases, sleep disorders,insomnia, hyperemotivity, neurosis. Benzodiazepines are only indicated in the treatment of anintense disorder that limits the patient’s activity or subjects him/her to significant stress.MianserineAntidepressant that blocks peripheral alpha-adrenoreceptors increasing the exchange ofnoradrenaline in the brain. It has slightly sedative, H1 antihistaminic and scarcely anticolinergicactivity. The following therapeutic indications have been approved in Spain: improvement ofdepressive symptoms in depression cases where pharmacological treatment is indicated. It is oneof the interventions in the control group of the RCTs studied in this CPG.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS246

MoclobemideMAOI antidepressant, mainly of the A subtype; decreases metabolism of noradrenaline, dopamineand serotonin, leading to greater extracellular concentrations of these transmitters. Its approvedtherapeutic indication in Spain is major depression.AdvocacyIn a social context, this technique is based on the influence on a person’s or group’s attitudestowards a specific matter.NaloxoneAntagonist of exogenously administered opioids. The following therapeutic indications have beenapproved in Spain: to totally or partially counteract respiratory depression caused by overdose ofnarcotics and dextropropoxifen or pentazocine, and also respiratory depression in the newborncaused by administration of opioids to the mother during delivery. Diagnosis when there issuspicion of acute narcotic intoxication.NaltrexoneAntagonist of exogenously administered opioids. The following therapeutic indications have beenapproved in Spain: alcoholism, opioid withdrawal, accompanied by other therapeutic measures.OlanzapineAntipsychotic, antimanic and mood stabiliser with an affinity for serotonin, dopamine, cholinergicmuscarinic, alpha-1-adrenergic and histamine receptors. The following therapeutic indicationshave been approved in Spain: schizophrenia, moderate or severe manic episode, relapseprevention of bipolar disorder whose manic episode has responded to olanzapine treatment,intramuscular administration for immediate management of agitation and disordered behavioursin schizophrenia or manic episode, when oral administration is not recommended.OndasentronPotent antiemetic antagonist that is highly selective of 5-HT3 receptors located in peripheralneurones and within the NCS. The following therapeutic indications have been approved in Spain:management of nausea and vomiting caused by chemotherapy and cytotoxic radiation therapy andpost-operative nausea and vomiting.OrlistatPeripherally acting drug designed to treat obesity.PimozideAntipsychotic drug that selectively blocks dopaminergic central receptors and has neurolepticproperties. The following therapeutic indications have been approved in Spain: acute and chronicpsychosis and anxiety disorders.247CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

PizotifenThis drug belongs to the group of antihistamines (whose effect is to block histamine H1 receptors).Aside from blocking the action of histamine H1 receptors in the brain, alleviating allergic reactionsymptoms, pizotifen is capable of blocking serotonin receptors in the brain, stimulating appetite.The following therapeutic indications have been approved in Spain: anorexia, thinness conditionedby psychic or “nervous” factors, weight deficit or loss, in puberty and senile patients.SibutramineAntidepressant. The following therapeutic indications have been approved in Spain:complementary therapy within a comprehensive weight management programme for patients withobesity (whose BMI is 30 kg/m 2 or more) and patients with overweight (whose BMI is 27 kg/m 2 ormore), who present other risk factors associated with obesity such as type 2 diabetes ordyslipidemia. It will be prescribed only to those patients who have not responded satisfactorily toan appropriate regimen that aims exclusively to tackle ponderal loss; that is, for patients whopresent difficulties in achieving or maintaining weight loss >5% in 3 months.Refeeding syndromeMetabolic disturbances and liquid and electrolyte imbalance with hypophosphatemia, cardiacinsufficiency, muscular weakness, immune and haematological dysfunction, digestive andnervous system disorders. It occurs when sudden refeeding is administered, with normal orexcessive caloric content, consisting mainly of carbohydrates. The best treatment for thissyndrome is to be aware of its existence and keep it in mind when refeeding a patient with aneating disorder. To tackle this syndrome, appropriate treatment will be based on the apparatus orsystem involved, modifying the route or load of deficitary micronutrients that are beingadministered (oral to parenteral, etc.).SulpirideSpecific dopamine D2 and D3 receptor antagonist anntipsychotic. The following therapeuticindications have been approved in Spain: diverse psychopathological pictures: neurosis,depression, neurotic somatizations, functional psychological disorders, psychosomatic syndromes,psychoasthenia, psychic involution of old age, gastrointestinal somatizations, vertigo. Inpsychiatry: acute psychotic, confusional, hallucinatory and delirious state, depressive state,schizophrenia, chronic delirium, autism, serious behavioural disorders, neurotic state withinhibition and depression and different cenestopathies.Induction-Dissonance TechniquesPrimary prevention psychosocial interventions that consist of performing exercises where eachparticipant targets one of his/her strongly-held belief and argues against this belief, to finddiscrepancies between both attitudes and promote effective change towards a new, betterstandpoint.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS248

Cognitive-Behavioural Therapy(CBT)Psychological therapy designed to enable people to establish links between thoughts, feelings oractions and current or past actions and reassess their perceptions, beliefs or reasoning on them.The interventions should include at least one of the following aspects: 1) control of thoughts,feelings or actions in relation to behaviour, 2) help in using alternative ways of addressingbehaviour, 3) reduce stress. A specific form of CBT has been developed for BN (CBT-BN) which,in general, involves 16-20 hours of individual sessions over four or five months. Its aim is not justto help patients modify eating habits, but also to cope with their patterns of thought (especiallyregarding the excessive value bestowed upon body shape and weight). CBT for patients with BED(CBT-BED) has been derived from CBT-BN.Behavioural Therapy (BT)Therapy that emphasises behavioural modification especially and not cognitive aspects as much.Systemic Family Therapy (SFT)FT is a form of psychotherapy that focuses on improving relationships and behavioural patternswithin the family as a whole, as well as between individual members and groups or subsystems inthe family. Systemic FT emphasises present relationships within the family and reassesses the roleof the designated patient, of the symbolic value and the secondary gain of the symptom for thefamily system. Another key feature of this approach is the contextualisation in the family of anyevent, action or judgement, where most things or events do not have an intrinsic value, but ratherare granted one depending on the function if fulfils within the system.Interpersonal Therapy (IPT)IPT was originally developed by Klerman, 1984, with the aim of being applied as maintenancetreatment after depression, although it was later used as independent treatment and, at present, itsuse has been extended to several different disorders. IPT mainly addresses current interpersonalrelationships and is focused on the patient’s immediate social contest: grief, interpersonaldisputes, role transition and interpersonal deficits. It has been adapted to BN treatment (IPT-BN;Fairburn, 1997). IPT-BN does not attempt to directly modify eating habits. Instead, it waits forthem to change by improving interpersonal behaviour. In the case of BED IPT-BN is adapted topatients with BED (IPT-BED).Psychodynamic Therapy (PDT)Type of psychotherapy based on psychoanalytical principles that consists of performing regularindividual therapy sessions with a trained psychotherapist, or under his/her supervision. A widerange of strategies is used, such as interventions aimed at understanding, support interventions ordirective activity.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS249

TopiramateAnticonvulsant psychoactive drug that blocks state-dependent sodium channels in neurones andboosts the potency of GABA activity. The following therapeutic indications have been approvedin Spain: epilepsy and migraine prophylaxis.TrazodoneAntidepressant. The following therapeutic indications have been approved in Spain: organic,psychogenic, symptomatic and involutive, combined states of depression and anxiety, atypical ormasked depressions (psychosomatic disorders), shakes, dyskinesia, mood/affective and behaviourdisorders (irritability, aggressiveness, emotional lability, apathy, tendency toward alienation,decreased sleep duration), preanesthetic, preendoscopic and postoperative medication.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS250

Annex 5. AbbreviationsABOS Anorectic Behaviour Observation Scale for parents/spouseACTA Attitude Towards Change in Eating Disorders (acronym in Spanish)ADANER Association in Defence of Anorexia Nervosa and Bulimia Management (acronym inSpanish)ADDH Attention Deficit Disorder with HyperactivityAGEMED Spanish Drug Agency (acronym in Spanish)AHRQ Agency for Healthcare Research and QualityAN Anorexia nervosaAPA American Psychiatric AssociationAR Assessment ReportBAT Body Attitude TestBED Binge eating disorderBDI or Beck Depression InventoryBES Body-Esteem ScaleBET Branched Eating Disorders TestBIA Body Image AssessmentBIS-11 Barratt Impulsiveness ScaleBITE Bulimia Investigatory Test EdinburghBMI Body Mass IndexBN Bulimia nervosaBPD Borderline Personality DisorderBSQ Body Shape QuestionnaireBT Behavioural TherapyCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS251

BULIT Bulimia TestBULIT-R Revised version of the BULITBWC Behavioural Weight ControlBWLT Behavioural Weight Loss TreatmentCAHTA Catalan Agency for Health Technology AssessmentCBT Cognitive-behavioural therapyCBT-BN Cognitive-behavioural therapy in bulimia nervosaCBT-BED Cognitive-behavioural therapy in binge-eating disorderCDI Children Depression InventoryCETA Assessment of Anxiety Disorders in Children and Adolescents (acronym in Spanish)ChEAT Children Eating Attitude TestChEDE-12 Children’s version of the EDE-12CI Confidence IntervalCIMEC Questionnaire on Influences of the Aesthetic Body Model (acronym in Spanish)CPG Clinical Practice GuidelinesCY-BOCS Children and Adolescent version of the Y-BOCSDH Department of Health, Day HospitalDM Diabetes mellitusDSM-IV-TR Diagnostic and Statistical Manual of Mental Disorders, fourth Edition, revisedtextEAT (EAT-40) Eating Attitudes TestEAT-26 Short version of the EAT-40ECG ElectrocardiogramED Eating DisorderEDDS Eating Disorder Diagnostic ScaleEDE-12 Semistructured interview, 12th edition (Eating Disorders Examination-12)252CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

EDE-Q Eating Disorders Examination-questionnaireEDI Eating Disorder InventoryEDNOS Eating Disorder Not Otherwise Specified (un-specific ED)ERP Exposure with response preventionES Effect sizeEU European UnionFEACAB Spanish Federation of Support Associations for Anorexia and Bulimia (from itsacronym in Spanish for Federación Española de Asociaciones de Ayuda y Lucha contra laAnorexia y la Bulimia)FT Non-specific Family TherapyGDG Guidelines Development GroupGM General recommendations for medical measuresGP General recommendations for psychological therapiesGPH General recommendations for pharmacological treatmentGSH Guided Self-HelpHAM-D Hamilton Depression Rating ScaleHARS Hamilton Anxiety Rating ScaleHIV Human Immunodeficiency VirusHRF Health Care Research Fund (the acronym in Spanish is FIS)IAS Health Care Institute (from its acronym in Catalan for Institut d’Assistència Sanitària)ICD-9 International Statistical Classification of Diseases and Related Health Problems, 9theditionICD-10 International Statistical Classification of Diseases and Related Health Problems, 10theditionINSALUD National Institute of Health (acronym in Spanish)IPDE International Personality Disorder ExaminationIPT-BN Interpersonal Therapy for bulimia nervosaIPT Interpersonal Therapy253CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

ISCIII Carlos III Health InstituteITP Individualised Treatment Plankcal Kilocalorieskg KilogramsMA Metaanalysis or quantitive reviewMACI Millon Adolescent Clinical InventoryMCMI-III Millon Multiaxial Clinical Inventory-IIIMHC Mental Health CentreMHCFA Mental Health Centre for AdultsMHCFCA Mental Health Centre for Children and AdolescentsMHGs Mutual Help GroupsMSC Ministry of Health and Consumer AffairsNC Nutritional counsellingNCCMH National Collaborating Centre for Mental HealthNHS National Health SystemNICE National Institute for Clinical ExcellenceNNT Number needed to treatNPV Negative Predictive ValueNSCM Non-specific Supportive Clinical ManagementOCD Obsessive-Compulsive DisorderPC Primary CarePDT Psychodynamic TherapyPPV Positive Predictive ValueQ-RCT Quasi-experimental RCTRCT Randomised controlled trial254CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

correlation coefficient rRR Relative RiskSCOFF Sick, Control, One, Fat, Food questionnaireSD Standard DeviationSED Survey for Eating DisorderssemFYC Spanish Society of Family and Community Medicine (from its acronym in Spanish forSociedad Española de Medicina de Familia y Comunitaria)SFP Supportive Focal PsychotherapySFT Systemic Family TherapySH Self-HelpSMD Standard Mean DifferenceSSRI Selective Serotonin Reuptake InhibibitorsSRSE Systematic Review Scientific EvidenceSTAI State-Trait Anxiety InventorySTAIC STAI’s version for childrenTCI-R Temperament and Character Inventory, revisedUB University of BarcelonaUK United KingdomUSA United States of Americavs. VersusY-BOCS Yale-Brown Obsessive-Compulsive Scale for OCDCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS255

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Annex 6. OthersAnnex 6.1. Protocols, recommendations, therapeutic orientationsand guides on eating disordersNATIONALCentral Catalonia Health Care Region. Catalan Health Service. Department of Health.Generalitat de Catalunya. Guia per a l'abordatge dels trastorns de la conducta alimentària aOsona; 2008 10 .semFYC. Working Group for the Prevention of Mental Health Disorders of the group forPreventive and Health Promotion Activities (PAPPS). Fernández Alonso MC, et al., Programade prevención en salud mental en atención primaria (fichas resumen). Primary Care; 2007 12 .Working Group for the Prevention of Mental Health Disorders of the PAPPS (approvedprogrammes). Fernández Alonso MC, et al., Programa de prevención en salud mental enatención primaria. Primary Care; 2005 13 . The complete text of the programmes is available onthe semFYC website (PAPPS): http://www.papps.org/upload/file/recomendaciones/2007/88-108_salud_mental.pdfEvidencia científica en soporte nutricional especializado. Intervention Manual of the Ministry ofHealth and Consumer Affairs. Madrid; 2006) 15 . Soldado M.Prevención primaria en TCA 4. Sevilla; 2006 149 .Primary Care and Mental Health Network of the Health Care Region of Girona. Department ofHealth. Catalan Health Service. Pilot plan for the management of eating disorders. Protocold’atenció integrat i específic en TCA. Girona; 2006 11 .Board of Graduate Studies. Spanish Physicians Association. Detecció i orientacionsterapèutiques en els trastorns del comportament alimentari. Good practice manuals. Barcelona;2005 17 .General Subdirectorate for Mental Health. Murcia Health Service. Guía práctica clínica de lostrastornos de conducta alimentaria. Murcia; 2005 16 .Hospital Universitario Príncipe de Asturias. Fernández Liria A, Diéguez Porres M. GuíaClínica para la atención a los TCA en el Área 3 de Madrid; 2005 150 .Consensus Committee of Catalonia on mental disorder therapeutics. Soler Insa PA, GascónBarrachina J. Recomendaciones terapéuticas en los trastornos mentales (RTMIII). Barcelona;2005 416 .CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS257

General Directorate for Public Health. Department of Health. Generalitat of Catalunya. Prats R,Prats B, Actuacions preventives a l’adolescència. Guia per a l’atenció primària de salut.Barcelona; 2004 146 .CatSalut. Department of Health. Generalitat of Catalunya. Serra J. Trastorns del comportamentalimentari. Guia per a l’atenció primària de salut. Barcelona; 2003 151 .CatSalut. Department of Health. Generalitat of Catalunya. Recomanacions per a l’atenció alsproblemes de salut mental més freqüents en l’atenció primària de salut. Health Plan. Booknumber. 11. Barcelona; 2000 417 .Ayuso Gutiérrez JL TCA. Psiquiatría en Atención Primaria [educational material]. Madrid;2000 147 .INSALUD. MSC. Moral Iglesias L. Trastornos del comportamiento alimentario. Criterios deordenación de recursos y actividades. Madrid; 2000 19 .MSC. González Briones E, Merino Merino B. Nutrición saludable y prevención de lostrastornos alimentarios. Madrid; 2000 148 .INSALUD. MSC. Protocolo de trastornos del comportamiento alimentario. Madrid;1995 20 .University Clinic. School of Medicine. University of Navarra. Cervera S, Gual MP, Lasa L, PratO, Zandio M, Hernández C., et al., Protocolo de atención a pacientes con TCA. Navarra;1995 418 .Clinical Guide AT. De enfermería a pacientes con TCA. Abordaje interdisciplinario de losTCA en atención primaria de salud [Internet monograph] (2008) 419 .Primary Care Management. Hospital Universitario “Lozano Blesa” Sector Zaragoza III. AragonHealth Service. Cobos A, Flordelís F, Gastón M, Pinilla M, Velilla M. TCA. Zaragoza (2008) 420 .INTERNATIONALOffice of School Food Services and Nutrition, South Carolina Department of Education,Columbia, SC, USA. Pilant VB. Position of the American Dietetic Association: local support fornutrition integrity in schools. 2006 421 .Royal College of Psychiatrists. York A, Lamb C, Editors. Building and sustaining specialistchild and adolescent mental health services. London; 2006 422 .NHS Quality Improvement Scotland. Eating disorders in Scotland: recommendations forhealthcare professionals. Consultation draft. Edinburgh; 2006 423 .CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS258

National Collaborating Centre for Mental Health. Obsessive-compulsive disorder: coreinterventions in the treatment of obsessive-compulsive disorder and body dysmorphic disorder.Leicester / London; 2006 424 .American Psychiatric Association. Work Group on Eating Disorders. Practice guideline for thetreatment of patients with eating disorders, third edition. Steering Committee on PracticeGuidelines, US; 2006 14 .Royal College of Psychiatrist. Guidelines for the nutritional management of anorexia nervosa.London; 2005 425 .American Academy of paediatrics. Promotion of healthy weight-control practices in youngathletes. Paediatrics. USA; 2005 426 .Finnish Medical Society Duodecim. “Eating disorders among children and adolescents” In: EBMGuidelines. Evidence-Based Medicine. Helsinki (Finland); 2004 427 .Royal Australian and New Zealand College of Psychiatrist Beumont P, Hay P, Beumont D,Birmingham L, Derham H, Jordan A, et al., Australian and New Zealand clinical practiceguidelines for the treatment of anorexia nervosa. New Zealand; 2004 18 .American Academy of Paediatrics. Identifying and treating eating disorders. Paediatrics.2003 428 .Unit for Child Psychiatry, University of Oulu, University Hospital of Oulu. Ebeling H,Tapanainen P, Joutsenoja A, Koskinen M, Morin-Papunen L, Jarvi L, et al., A practice guidelinefor treatment of eating disorders in children and adolescents. Finland; 2003 429 .Council for Nutritional Strategies in Long-Term Care. Thomas DR, Ashmen W, Morley JE,Evans WJ. Nutritional management in long-term care: development of a clinical guideline.Missouri US; 2000 430 .Annex 6.2. Results of the search, selection and qualityassessment of the evidence based on the stages performed1) 115 documents were identified: guidelines, reviews and ARs. After applying selectioncriteria (to the title and/or abstract), 73 were excluded. The complete document of all 42retrieved documents (14 were potential guidelines) was requested. After review, 28 more wereexcluded (11 of them for not being considered guidelines 421-431 ) and 15 were included (314, 18guidelines and 12 reviews). After assessing the quality with specific instruments, 2 CPGsand 11 reviews were excluded. Only two documents met quality criteria: one NICE CPG 30 andone AHRQ SRSE 31 . The evidence tables in the different chapters state the quality of each SRSE.That is not the case in the only quality CPG, which is described solely as CPG.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS259

2) We identified 20 documents elaborated in our setting relating to protocols, recommendations,therapeutic orientations and guidelines on eating disorders developed by institutions of the healthadministration, scientific societies, hospitals and other organizations in our setting. None ofthese documents met the quality criteria established by the working group and were thusexcluded 10-13, 15-17, 19, 20, 146-151, 416-420, .3) Of the documents retrieved, 12 RCTs 140, 145, 203, 238, 253, 254, 274, 316, 318, 319, 331, 432 were included, theirquality being 1++ (9) and 1+ (3). The rest were excluded due to topic, language ormethodology. One quality 1++ RCT was manually identified 320 .4) Of the documents identified in the CPG/SRSE/AR, 14 SRSE were included based on titleand/or summary. After reviewing the entire document, 7 137,202, 211, 245, 308, 397, 433were included and the other 7 434-440 were excluded for not being considered SRSE.The quality of all 7 SRSE included is 1++ 137, 202, 211, 245, 308, 397, 433 . No guidelines were identified.5) Of the documents identified on primary prevention, 14 SRSE, 103 RCTs and 1 guideline,which was excluded due to its low quality, were retrieved. 8 SRSE 134-136, 441-445 were preliminarilyselected based on their title and/or summary. Excluded SRSE included one that had beenidentified and included in the previous search 137 441-443, 445. After reviewing the entire document, fourwere excluded (one due to its date and three due to low quality), 3 were included (quality 1++) 134-136and the original version 444 of an already included SRSE 137 was excluded. Of the identifiedRCT, 51 RCTs were excluded (language or topic) and 52 were preliminarily included, of which38 are included in one of the quality SRSE included 137 and two were repetitions. The entiredocument of the remaining 12 RCTs and 2 manually identified ones was reviewed, resulting inthe inclusion of 8 RCTs 138-145 .6) Different reviews and articles on the topic have been identified, on which the prognosischapter is based.7) In the consultation of these different sources, one SRSE of the Cochrane Collaboration on SHand GSH in eating disorders 257 was identified. Another Cochrane Collaboration was excludeddue to its date 446 .Annex 6.3. Description of the NICE CPG (January, 2004) 30Title: Eating disorders. Core interventions in the treatment and management of anorexianervosa, bulimia nervosa and related eating disorders.Developed by: National Collaborating Centre for Mental Health (NCCMH). The developmentgroup of the CPG (GDG) was selected by the e NCCMH. The GDG is composed by:psychiatrists, clinical psychologists, nurses, social workers, general physicians, an eatingdisorder association representative and a patient. The GDG received technical support from staffmembers of the NCCMH in the search and summarising of the scientific evidence. NICE staffadvised the GDG on the development process of the CPG.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS260

Commissioned and Published by: National Institute for Clinical Excellence (NICE) and TheBritish Psychological Society and The Royal College of Psychiatrists, respectively, January2004.Target population: Eating disorders (AN, BN and BED).Scope: aimed at all patients with AN, BN and related eating disorders, who are aged 8 years andolder. The CPG does not include all mental health or physical pathologies in which an eatingdisorder is a symptom.Potential users: scientific associations, health care professionals, researchers, planners, familymembers and educators.Funding: NICE.Methodological Aspects:1) Search for evidenceSRSE in English published or updated after 1995. The search was completed with RCT andother designs. The quality of the SRSE was determined by parallel independent assessment. Theselection and assessment of quality was tested in a representative group of documents. Theguide includes the general and specific search filters developed by the reviewer group.Electronic searches were carried out in the main bibliographic databases: MEDLINE, EMBASE,CINAHL and PSYCINFO. Also in the Cochrane Database of Systematic Reviews, the NHSR&D Health Technology Assessment database, Evidence-Based Mental Health and ClinicalEvidence (Issue 5). In order to include evidence published after search dates, evidence identifiedby experts was reviewed, including reference lists and recent summaries of selected journals.When no SRSE were found, new searches were performed in compliance with the GDG’sdecision.2) Quality and Strength of the EvidenceIntervention studies were classified in accordance with the accepted hierarchy of evidence: Levelof evidence (I, IIa, IIb, III and IV) and grade of recommendation (A, B and C) depending on thetype and level of respectively associated evidence.The levels of evidence of the NICE guide scale correspond to the following levels of the SIGNscale: I=1++; IIa=1+; IIb=1-; III=2 (-, +, ++) and IV=3, 4. A and B grades of recommendationcoincide in both the NICE scales and the SIGN scale used in this CPG. The C grade of theNICE scale could be extrapolated to the D grade of the SIGN scale.When statistically significant results were obtained after controlling heterogeneity, the GDGassessed whether these findings were clinically significant (for example, if benefit for patientswas probable) taking the RCT population, the nature of the outcome and effect size (ES) intoaccount. On this basis, effect size was considered clinically significant or not. The next stepwas to assess the strength of the evidence, by examining the confidence intervals of the effectCLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS261

estimator, establishing the following categories: S1= strong evidence (clinically significant ESand CI with a range of clinical relevance (level of evidence I); S2= limited evidence (not a levelof evidence I or situations where one of the CI extremes is not clinically significant); S3=unlikely that it is clinically significant, if it is not a level of evidence I or if ES is statistically butnot clinically significant, and the CI excludes clinically important values; S4= when the ES isnot statistically significant: if the CI is narrow and excludes a clinically significant ES, thedifference is not considered to be clinically significant; S5= but if the CI is wide, it is consideredinsufficient evidence to determine if there was a clinically significant difference or not. S6= ifthe CI includes clinically important values, it is considered insufficient to determine clinicalsignification.3) Method to formulate recommendationsThe importance of acknowledging that the grade of recommendations does not always reflecttheir clinical significance or relevance is emphasised.Annex 6.4. Description of the AHRQ’S SRSE (April, 2006) 31Title: Management of Eating Disorders.Developed by: RTI-UNC Evidence-Based Practice Centre, Research Triangle Park, NC (centreascribed to the AHRQ). The GDG of this guide was advised by and received feedback from atechnical experts panel (TEP) comprised of 11 people, mainly psychiatrics from differentsettings and one family representative. 23 external reviewers, some from the TEP, alsoparticipated.Commissioned and Published By: Agency for Healthcare Research and Quality (AHRQ),USA. AHRQ Publication Nº 06-E010, April 2006.Target Population: AN, BN and EDNOS.Scope: treatment of eating disorders (efficacy, adverse effects, factors associated with treatmentefficacy, sex-, age-, race-, ethnic group- or cultural group-related differences in treatmentefficacy, factors associated with outcomes and sex-, age-, race-, ethnic group- or cultural grouprelatedoutcome differences).Results of Interest: eating-related behaviours, psychiatric or psychological outcomes andbiomarkers.Potential Users: scientific associations, health care professionals, researchers and planners.Funding: Office of Research on Women’s Health (NIH).Methodological Aspects:1) Search for Evidence262CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS

Consulted bibliographic databases: MEDLINE, Cumulative Index to Nursing and AppliedHealth (CINAHL), PSYCHINFO, Educational Resources Information Centre (ERIC), NationalAgricultural Library (AGRICOLA) and Cochrane Collaboration Libraries. The guide includesthe search performed. Study inclusion criteria: published in all languages, between 19080 andSeptember 2005, in humans aged 10 years and older, of both sexes, diagnosed mainly with AN,BN or BED and informing on at least one of the relevant results.2) Selection of the EvidenceA reviewer carried out the application of selection criteria to titles and/or summaries. Excludedsummaries were assessed by another expert reviewer, and reasons for exclusion were classified.3) Quality Assessment and Synthesis of the EvidenceEvidence tables were elaborated; an external reviewer extracted data on treatments and results;another reviewer confirmed that they were exact, complete and consistent; both reconcileddisagreements. Each reviewer assessed the quality of the studies. The analysis was focused onstudies qualified as moderate (1+) or high (1++) quality.4) Quality and Strength of the Evidence according to West, et al. (2002) 4472 forms were developed to assess the quality of the studies about treatment (25 items) and results(17 items) that enabled the classification of quality as low, moderate or high. The body ofevidence was graded for each key question based on three dimensions: study quality, results andconsistency of findings. After consensus of three expert researchers, the following levels ofevidence were defined: I=strong, II=moderate, III=weak and IV=no evidence.CLINICAL PRACTICE GUIDELINE FOR EATING DISORDERS263

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